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146 publications mentioning hsa-mir-152 (showing top 100)

Open access articles that are associated with the species Homo sapiens and mention the gene name mir-152. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

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[+] score: 350
We aim to address the following questions: (1) Whether β-catenin is direct target of miR-152 in breast cancer; (2) whether miR-152 overexpression inhibits cell proliferation by inhibiting both β-catenin and PKM2 expression; (3) what is role of miR-152 in breast cancer resistance to paclitaxel treatment; (4) whether miR-152 is involved in IGF-1 -induced β-catenin and PKM2 expression. [score:14]
MiRNAs are a class of small endogenous non-coding RNAs composed of 17–24 nucleotides that act as post-transcriptional regulators through directly binding to the 3′-untranslated region (3′ UTR) of their target mRNAs, resulting in the degradation or translational inhibition of the mRNAs 3, 4. MicroRNA-152 (miR-152) contains two different mature miR-152 sequences, namely miR-152-5p and miR-152-3p. [score:11]
Additionally, we observed that expression levels of PKM2 were downregulated in miR-152 stable expressing cells, and were restored in cells with forced expression of PKM2 without 3′UTR (Fig.   2F). [score:10]
To assess whether miR-152 suppressed β-catenin expression by directly targeting its 3′UTR region, we established MCF7 and MDA-MB-231 cell lines stably expressing miR-152 or miR-NC using lentiviral transduction. [score:10]
Overexpression of β-catenin and PKM2 was observed both in TNBC and TPBC tissues, but not in NBT tissues, while miR-152 levels were much higher in NBT, and lower or non-expressed in TPBC and TNBC tissues, confirming that expression levels of miR-152 were inversely correlated with the β-catenin and PKM2 expressions levels in these tissues (Table  1). [score:9]
To further examine the reduction of β-catenin transactivation by miR-152, TCF/LEF-1 luciferase reporter analyses showed that force expression of miR-152 significantly inhibited β-catenin transactivation while downregulation of miR-152 by using anti-miR-152 promoted β-catenin transactivation (Fig.   1E). [score:8]
Furthermore, DNA methyltransferase 1 (DNMT1), a target of miR-152, mediated CpG island hypermethylation of miR-152 gene promoter that may suppress miR-152 expression as a feedback regulatory mechanism [10]. [score:8]
In addition, to test whether miR-152 downregulates the expression of β-catenin, we transfected negative control (miR-NC) or miR-152 mimics into MCF7 and MDA-MB-231 cells, then detected β-catenin expression at the protein level. [score:8]
It was observed that overexpression of miR-152 significantly sensitized the breast cancer cells to paclitaxel treatment; however, the chemotherapy sensitivity due to miR-152 overexpression was significantly reversed by overexpression of PKM2. [score:7]
Moreover, downregulation of PKM2 or β-catenin abrogated the IGF-1 -induced miR-152 expression, suggesting that miR-152 was involved in a new IGF-1 -mediated miR-152/PKM2/β-catenin regulatory circuit in breast cancer. [score:7]
Immunoblotting results showed that miR-152 overexpression was sufficient to inhibit β-catenin protein expression (Fig.   1D). [score:7]
Overexpression of miR-152 significantly repressed PKM2, β-catenin, IGF-1R and IRS-1 expressions, but not GSK3β, which was not a target of miR-152 (Fig.   5D). [score:7]
The results demonstrated that overexpression of PKM2 rescued miR-152 -inhibited cell proliferation (Fig.   2G) and colony formation (Fig.   2H), confirming that PKM2 was also an important target of miR-152 for breast cancer cell proliferation and colony formation. [score:7]
Taken together, these data provide evidence that miR-152 may act as tumor suppressor in breast cancer cells by inhibiting cell growth and colony formation via inhibiting both β-catenin and PKM2. [score:7]
Overexpression of miR-152 significantly inhibited cell proliferation, colony formation and tumor angiogenesis by targeting IGF-1R and IRS1 in breast cancer. [score:7]
Taken together, our results reveal the vital role of miR-152 as a tumor suppressor in human breast cancer by inhibiting both β-catenin and PKM2 expression levels at the post-transcriptional level, and point out the potential clinical application of miRNA-analog for the cancer treatment. [score:7]
To further understand molecular mechanism of miR-152 in breast cancer cells, several well-developed miRNA algorithms, such as TargetScan, miRNApath, and TargetSearch, were employed to obtain a list of possible mRNA targets of miR-152. [score:7]
Except for DNMT1, accumulating evidence indicates that miR-152 targets on multiple oncogenes like PKM2, IRS-1 and IGF-1R in human breast cancer, and inhibits a variety of cellular functions, including proliferation, angiogenesis and migration, suggesting that miR-152 may potentially function as a tumor suppressor in breast cancer 8, 10, 14. β-catenin, the downstream molecule of IGF-1 15, 16, is originally identified as an important junctional component at the cell membrane, where it serves to link cadherin to the actin cytoskeleton via binding of α-catenin [17]. [score:7]
Moreover, miR-152 -suppressed β-catenin expression was reversed by forced expression of β-catenin (Fig.   2B). [score:7]
We also interfered IGF-IR in breast cancer cell lines and the results showed that miR-152 expression level was inhibited by IGF-1R knockdown (Supplementary Figure  S2). [score:6]
In addition, IGF-1 incubation significantly induced expression levels of miR-152 in MCF7 cells, but not in MDA-MB-231 cells; while depletion of PKM2 or β-catenin partly abrogated the IGF-1 -induced miR-152 upregulation in MCF7 cells, but not in MDA-MB-231 cells (Fig.   5E). [score:6]
Our previous studies explored that miR-152 inhibited the Warburg effect by directly targeting PKM2 [14]; while β-catenin had been reported to be an interacting protein of PKM2 in various cancer cells dependent on EGF stimulation. [score:6]
However, IGF-1 -induced upregulation of miR-152 expression was not observed in MDA-MB-231 cells. [score:6]
It was reported that the miR-152 directly targeted DNMT1 (DNA methyltransferase 1) in malignant cholangiocytes, leading to significant reduction of DNMT1 expression at both mRNA and protein levels [11]. [score:6]
Cell proliferation was inhibited in miR-152 -overexpressing MCF7 and MDA-MB-231 cells compared with miR-NC -overexpressing cells. [score:6]
Previous study indicated that miR-152 directly targeted and inhibited PKM2 in breast cancer [14]. [score:6]
Thus, the suppression of β-catenin by miR-152 was functionally validated, suggesting that miR-152 specifically targeted β-catenin by binding its seed sequence to β-catenin 3′UTR region. [score:5]
The expression level of miR-152 (normalized to U6) in MCF7 and MDA-MB-231 cells stably overexpressing miR-152 or negative control of miRNA (miR-NC) were analyzed by qRT-PCR. [score:5]
Correlation of miR-152 suppression, β-catenin and PKM2 overexpression in clinical breast cancer tissues. [score:5]
Our results showed that forced expression of β-catenin restored miR-152 -inhibited colony formation (Fig.   2D). [score:5]
Moreover, miR-152 significantly inhibited protein expression and transactivation of β-catenin. [score:5]
To test miR-152 expression levels in breast cancer tissues, quantitative real time PCR (qRT-PCR) analysis was performed to detect miR-152 expression levels in 18 pairs of breast cancer tissues and matched adjacent normal breast tissues. [score:5]
These results indicated the highly negative correlations between expression levels of miR-152 and its target proteins: β-catenin and PKM2 in human breast cancer tissues. [score:5]
Although multiple miRNAs, such as miR-122 [30], miR-18b [31], miR-515-5p [32], miR-148a and miR-152 10, 14, are involved in IGF-1 regulation pathway by directly targeting IGF-1, IGF-1R, IRS-1 or FOXO3a in breast cancer, the effects of IGF-1 induced signaling cascades on miRNA expression in breast cancer has yet to be evaluated. [score:5]
Similarly, the suppression of miR-152 expression also occurred in breast cancer cell lines MCF7, T47D, MDA-MB-231, MDA-MB-453 when compared with immortalized breast epithelial MCF-10A cells by qRT-PCR (Fig.   1B). [score:4]
MiR-152 downregulation is associated with breast cancer development. [score:4]
Importantly, cell proliferation suppressed by miR-152 was rescued by overexpression of β-catenin cDNA without 3′UTR in MCF7 and MDA-MB-231 cells when compared with control group (Fig.   2C). [score:4]
In the present study, we showed that miR-152 was downregulated in breast cancer. [score:4]
Then, colony formation assay was performed to test whether β-catenin forced expression is sufficient to restore miR-152 -inhibited cell transformation. [score:4]
Cells overexpressed miR-152 showed low expression levels of β-catenin protein when compared with those of negative control cells. [score:4]
Given the important role of β-catenin in regulation of cell proliferation 22, 33– 35, miR-152 overexpressed MCF7 and MDA-MB-231 cells were used to analyze cell proliferation. [score:4]
Our results confirmed that miR-152 was downregulated in both breast cancer tissues and cancer cell lines. [score:4]
The results showed that the expression levels of miR-152 were significantly decreased in breast cancer tissues than those in noncancerous tissues (Fig.   1A). [score:3]
In this study, our results identified β-catenin as a new target of miR-152. [score:3]
The miR-152 -overexpressing MCF7 and MDA-MB-231 cell lines were constructed by using a lentiviral packaging kit. [score:3]
Then these miR-NC or miR-152 stably expressing cells were transfected with β-catenin and PKM2 cDNA constructs without 3′UTR region. [score:3]
MiR-152 is downregulated in breast cancer tissues and cell lines. [score:3]
MCF7 and MDA-MB-231 cells stably overexpressed miR-152 were transfected with β-catenin or PKM2 cDNA plasmid. [score:3]
Our results showed that IGF-1 significantly increased the expression levels of β-catenin and PKM2, enhanced their interaction, and promoted their nuclear accumulation, thus leading to miR-152 transcriptional activation. [score:3]
MiR-152 directly targets β-catenin in breast cancer cells. [score:3]
As shown in Fig.   1C, the luciferase activity of β-catenin WT 3′UTR was reduced by miR-152 overexpression, whereas the Mut constructs activity was not affected. [score:3]
Recently, decreased expression of miR-152-3p (here referred as miR-152) has been observed in various types of human cancer cell lines and tumor tissues, such as ovarian [6], gastrointestinal cancer [7], hepatocellular carcinoma [8], endometrial [9] and breast cancer [10]. [score:3]
We predict that miR-152 simultaneously targets both PKM2 and β-catenin in breast cancer cells. [score:3]
Additionally, the lower miR-152 expression level in MDA-MB-231 cells may be related to the hypermethylation of miR-152 gene promoter. [score:3]
Our data showed that miR-152 sensitized breast cancer cells to paclitaxel treatment by targeting β-catenin and PKM2 repression, suggesting a novel role of miR-152 in breast cancer paclitaxel resistance. [score:3]
Similarly, cell proliferation and colony formation were used to examine the involvement of PKM2 in miR-152 -inhibited effects in the two different breast cancer cell lines. [score:3]
Additionally, overexpression of β-catenin in these cells also partially reversed the paclitaxel sensitivity, demonstrating that both of PKM2 and β-catenin are involved in miR-152 -induced paclitaxel treatment response and PKM2 played a more sensitive role in paclitaxel resistance of breast cancer (Fig.   3). [score:3]
Figure 6The miR-152 expression levels was negatively correlated to β-catenin and PKM2 levels in breast cancer patients. [score:3]
The expression levels of miR-152 were analyzed in these stable cell lines using qRT-PCR (Fig.   2A). [score:3]
Subsequently, IGF-1 -induced PKM2 and β-catenin complex translocates into nucleus, which in turn activates the expression of miR-152. [score:3]
Next, we examined β-catenin, PKM2 and miR-152 expression levels in 25 pairs of breast cancer specimens and their matched adjacent normal breast tissues (NBT), including 9 triple negative breast cancer (TNBC) tissues and 16 triple positive breast cancer (TPBC) tissues by using In situ hybridization and Immunohistochemical staining (Fig.   6B). [score:3]
MiR-152 sensitizes the breast cancer cells to paclitaxel treatment by decreasing β-catenin and PKM2 expression. [score:2]
MiR-152 represses cell growth by both targeting β-catenin and PKM2. [score:2]
The answer of these questions would provide new insights into a better understanding of the role of miR-152 in breast cancer development. [score:2]
[#]Indicates p < 0.05 when compared to miR-152 overexpression group. [score:2]
In situ hybridization Slides were treated and hybridized with 10 pmol probe (LNA -modified and DIG labeled oligonucleotide) complementary to miR-152, according to the manufacturer’s instructions. [score:1]
Pearson Correlation analysis showed the significant negative correlations between miR-152 and PKM2 (correlation = 0.−315, p = 0.026), and β-catenin (correlation = 0.−286, p = 0.044), respectively. [score:1]
Thus, the combination treatment of miR-152 with paclitaxel could provide a new strategy to overcome paclitaxel resistance in breast cancer in the future. [score:1]
The 3′-UTR regions of β-catenin and PKM2 containing predicted miR-152 seed-matching sites (wide type, WT; mutant type, Mut) were inserted into pMIR-GLO vector (Ambion, CA, USA). [score:1]
*Indicates p < 0.05 when compared to miR-NC group; [#]indicates p < 0.05 when compared to miR-152 overexpression group. [score:1]
It is possible that the hypermethylation of CpG islands in miR-152 gene promoters were found in MDA-MB-231 cells, which may abrogate the binding of many transcription factors, such as EGR1 [14]. [score:1]
After cultured overnight, cells were cotransfected with the WT or Mut plasmid and equal amounts of miR-152 or miR-NC using Lipofectamine 2000 (Invitrogen) according to the manufacturer’s instruction. [score:1]
As a potential miR-152 binding site was predicted within the 3′-UTR of β-catenin mRNA, we constructed the 3′UTR reporters of β-catenin containing the miR-152 binding sites (WT) and corresponding mutant constructs (Mut) with 3 base pair substitution downstream of the pMIR-GLO luciferase reporters. [score:1]
The expression level of miR-152, PKM2 and β-catenin in breast cancer cells and tissues were measured by quantitative real time RT-PCR (qRT-PCR). [score:1]
Negative control (miR-NC) or miR-152 mimics (200 μM and 400 μM) were transiently transfected into MCF7 and MDA-MB-231 cells for 48 hours. [score:1]
In addition, miR-152 plays an important role in breast cancer cell proliferation and angiogenesis via PKM2/NF-κB/EGR1/miR-152 complex in respond to IGF-1R activation [14]. [score:1]
Slides were treated and hybridized with 10 pmol probe (LNA -modified and DIG labeled oligonucleotide) complementary to miR-152, according to the manufacturer’s instructions. [score:1]
Lentivirus carrying hsa-miR-152 or hsa-miR-NC was packaged following the manufacturer’s manual. [score:1]
Therefore, we performed studies to identify the known binding site of miR-152 in PKM2 3′UTR region. [score:1]
The objective of this study was to reveal the molecular mechanism of miR-152 and β-catenin in breast cancer. [score:1]
The luciferase activity of PKM2 3′UTR WT reporter, but not Mut reporter was significantly reduced in the cells transfected with miR-152 (Fig.   2E). [score:1]
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[+] score: 271
Moreover, we co -transfected gastric cancer cell lines with specified miR-152 inhibitor and mimic and found that could restore expression of B7-H1 in gastric cancer cell lines (Figure 4), which indicated miR-152 can specifically inhibit expression of B7-H1. [score:9]
Inhibition of miR-152 expression enhanced B7-H1 expression. [score:7]
Figure 4MiR-152 inhibitor can significantly inhibited B7-H1 mRNA expression with co-transfection of miR-152 mimic in SGC-7901 (A) and AGS (B). [score:7]
MiR-152 inhibitor can significantly inhibited B7-H1 mRNA expression with co-transfection of miR-152 mimic in SGC-7901 (A) and AGS (B). [score:7]
Therefore, we confirmed that miR-152 could bind directly to B7-H1 3′-UTR region and inhibit B7-H1 expression. [score:6]
Collectively, all these data indicated that expression of B7-H1 is inhibited by miR-152 and thus loss miR-152 may result in development of cancer T cells is important in immunologic surveillance and loss of function of T cells may lead to tumor immune escaping [26]. [score:6]
And co-transfection of miR-152 mimic with inhibitor showed inhibition of T cells proliferation compared to transfection of miR-152 mimic with scramble inhibitor group. [score:6]
Song et al. found that miR-152 inhibited gastric cancer cells proliferation by targeting cholecystokinin-B receptor [21]. [score:5]
Zhai et al. reported miR-152 suppresses gastric cancer cell proliferation via targeting CD151 [22]. [score:5]
org) to screen target genes of miR-152 and found B7-H1 is putative target of miR-152. [score:5]
B7-H1 expression was inhibited by transfection of miR-152 mimic in gastric cancer cell lines. [score:5]
Also, expression B7-H1 was increased by co-transfection with miR-152 mimic and inhibitor in AGS cell line (F– H). [score:5]
Before co-culture, SGC-7901 was transfected with miR-152 mimic, inhibitor or mimic and inhibitor for 48 hours according to manufacturer's protocol then IFN-γ (20 ng/ml) was added for another 24 hours. [score:5]
Similarly, transfection of mimic of miR-152 significantly augmented interleukin-2 (IL-2) and IFN-γ production and co-transfection of miR-152 mimic with inhibitor inhibited rate of IL-2 and IFN-γ positive T cells (Figure 6C–6F). [score:5]
Inh means miR-152 inhibitor; Inh con means miR-152 inhibitor control. [score:5]
Flow Cytometry (C and D) and Western blot (E) showed that miR-152 inhibitor increased expression of B7-H1 with co-transfection of miR-152 mimic in SGC-7901. [score:5]
These finding suggested that miR-152 inhibited B7-H1 expression. [score:5]
Also, expression B7-H1 was inhibited by transfection with miR-152 mimic in AGS cell line (F– H). [score:5]
As shown in Figure 4, co-transfection of specified inhibitor and miR-152 mimic can significantly increase B7-H1 mRNA expression. [score:5]
Subsequently, enforced miR-152 expression enhanced T cells proliferation and function via targeting immune checkpoint molecular B7-H1. [score:5]
MiR-152 inhibited expression of B7-H1 in gastric cancer cell lines. [score:4]
In present study, transfection of miR-152 can significantly restore proliferation of T cells, suggesting that miR-152 have a direct effect on immune response by decreasing expression of B7-H1, which can be explored therapeutically (Figure 6). [score:4]
B7-H1 is a direct target of miR152. [score:4]
MiR-152 could bind with 3′-UTR of B7-H1 and inhibited its expression. [score:4]
As shown in Table 1, we found that the low expression of miR-152 was associated with tumor size, stage and positive lymph node metastasis. [score:3]
Cytokines (IFN-γ and IL-2) production increased after co-cultured with gastric cancer cells (SGC-7901) transfected of miR-152 mimic and decreased after co-cultured with cells co -transfected with specified miR-152 inhibitor with mimic (C– F). [score:3]
All those indicated that miR-152 increased immune response by inhibiting B7-H1. [score:3]
As shown in Figure 5, luciferase activity was significantly inhibited when cells were transfected with miR-152 mimic and Luc-B7-H1 vector. [score:3]
Here we used miR-152 mimic and inhibitor to co-transfect AGS and SGC-7901 cells. [score:3]
The expression of microRNA-152 and mRNAs level were determined based on CT value and normalized to U6 or GAPDH levels, respectively. [score:3]
24 hours later, cells were cotransfected with miR-152 mimic or mimic control (scrambled control miRNA) with empty control vector or expression vectors containing luciferase gene fused to the wild type (WT) or mutant miR-152 binding site B7-H1 3′UTR (RiboBio, Guangzhou, China) using HiPerFect Transfection Reagent (Qiagen, Hilden, Germany). [score:3]
Transfection of miR-152 mimic restored T cells proliferation (B) and co-transfection specified miR-152 inhibitor with mimic can eliminate such effect (B). [score:3]
Here we found that transfection of miR-152 mimic reduced B7-H1 expression in SGC-7901 and AGS gastric cell lines (Figure 3). [score:3]
As expression of B7-H1 was negatively correlated with miR-152 levels in gastric cancer. [score:3]
To confirm whether B7-H1 is a direct target of miR-152 in GC cells, the luciferase report assay was performed. [score:3]
Previous studies have demonstrated that miR-152 acts as a tumor suppressor [21, 22, 24, 25]. [score:3]
inhibition of miR-152 increased level of B7-H1 in gastric cancer cells. [score:3]
Moreover, the association between expression of miR-152 and expression of GC immune check point was evaluated. [score:3]
Therefore, low expression of miR-152 is involved in carcinogenesis in gastric cancer. [score:3]
The relationship between the expression of miR-152 and clinicopathologic features was analyzed by χ2 tests. [score:3]
Next, we tried to explore whether B7-H1 is potential target of miR-152. [score:3]
There was a significant reduction of B7-H1 mRNA expression with transfection of miR-152 mimic in SGC-7901 (A) and AGS (B). [score:3]
Correlation between miR-152 and mRNA expression levels of B7-1, B7-2, B7-H1 and B7-H3. [score:3]
We found that there was a significant inverse correlation between miR-152 and B7-H1 expression in gastric cancer samples (Figure 2). [score:3]
Hence we speculated that miR-152 might be associated with expression of B7-H1 in gastric cancer. [score:3]
MiR-152 was reported down regulated in gastric cancer tissues compared to matched normal tissues and low expression of miR-152 was correlated with increased tumor sizes and stage [23]. [score:3]
MiRNA-152 mimic and inhibitor were used to explore the specific interaction between miR-152 and B7-H1. [score:3]
Expression of miR-152 in gastric cancer patients and cell lines. [score:3]
Therefore, the miR-152 may have therapeutic potential to increase immune response, as well as to inhibit growth of tumor in gastric cancer. [score:3]
Inh con means miR-152 inhibitor control; Carboxyfluorescein succinimidylester (CFSE). [score:3]
Figure 3There was a significant reduction of B7-H1 mRNA expression with transfection of miR-152 mimic in SGC-7901 (A) and AGS (B). [score:3]
The miR-152 expression level in cancer tissues and its mormal control were analyzed by Student's t-test. [score:3]
Our finding from present study defined a new role for miR-152 and suggested that miR-152 specifically activates immune response via targeting B7-H1. [score:3]
miR-152 expression and clinicopathologic factors. [score:3]
Here we detected whether miR-152 was able to increase T cells function by inhibiting B7-H1. [score:3]
Flow Cytometry (C and D) and Western blot (E) demonstrated that there was a marked reduction of expression of B7-H1 with transfection of miR-152 mimic in SGC-7901. [score:3]
We found expression of miR-152 was correlated with level of B7-H1. [score:3]
Expression of miR-152 was decreased in gastric cancer tissues and cell lines compared to non-tumor control. [score:2]
MiR-152 increased T cells proliferation and function via inhibition of B7-H1. [score:2]
Our results therefore suggests miR-152 is a potential prognostic and therapeutic marker for gastric cancer and identify a novel mechanism by which tumor immune response is regulated by miR-152 via B7-H1. [score:2]
As shown in Figure 1B, expression of miR-152 decreased markedly in five gastric cancer cell lines (AGS, MKN-45, BGC-803, GC-7901, and BGC-823) compared to normal gastric epithelium cell line (GES-1). [score:2]
MiR-152 restored T cells function via inhibition of B7-H1. [score:2]
It is likely that further research into microRNA-152 might shed the light on the development of drug and therapeutic strategies for treatment of gastric cancer. [score:2]
The WT B7-H1 3′-UTR+miR-152 group showed significant reduction of luciferase activity (B). [score:1]
We divided all gastric cancer patients into two groups according to ratio of tumor/normal of miR-152. [score:1]
However, a limitation for this study is the fact that an investigation of correlation between miR-152 expression and patients’ survival is needed. [score:1]
From our results, we revealed new function of miR-152 and displayed that miR-152 can reactivate T cells response in vitro. [score:1]
Furthermore, dual-luciferase reporter assay demonstrated that miR-152 can directly bind with 3′-UTR of B7-H1. [score:1]
Figure 2(A) There was significant correlation between miR-152 and B7-H1 mRNA level (p < 0.05, r = −0.51). [score:1]
Among them, SGC-7901 and AGS displayed the most reduction of miR-152. [score:1]
There was no significant correlation between miR-152 and mRNAs level of B7-H3 (B), B7-1 (C) and B7-2 (D). [score:1]
Lower miR-152 is associated with poor stage, increasing tumor size and higher positive lymph node metastasis. [score:1]
However, we did not found any correlation between miR-152 and patient's age, gender, liver metastasis and tumor location. [score:1]
In our study, first we investigated expression of miR-152 in surgically resected human GC tissue and several GC cells lines. [score:1]
However, co-transfection with miR-152 mimic scramble control and Luc-B7-H1 vector or empty vector showed no significant effect to luciferase activity. [score:1]
Correlations among miR-152, B7-H3, B7-H1, B7-1 and B7-2 mRNA Levels in gastric cancer patients. [score:1]
There were evidences that miR-152 was associated with gastrointestinal cancer. [score:1]
We co -transfected SGC-7901 with miR-152 and a reporter vector encoding luciferase which is fused with 3′-UTR of B7-H1 gene (Luc-B7-H1 vector). [score:1]
In the present study, lower miR-152 level was significantly related to clinicopatholgic parameters such as increasing tumor size, advanced pT stage and higher lymph node metastasis rate (Table 1). [score:1]
In conclusion, our study provided data that miR-152 was significantly decreased in gastric cancer tissues and cell lines. [score:1]
In addition, we measured expression of miR-152 level in cell lines. [score:1]
However, the involvement of miR-152 in tumor immune is still poorly understood. [score:1]
In accordance with the recovery of proliferation, the production of cytokines including IFN-γ and interleukin-2 were increased by transfection of miR-152 mimic (Figure 6). [score:1]
MiR-152 reduced luciferase activity via directly binding to 3′-UTR of B7-H1. [score:1]
Then the association of expression of miR-152 and clinicopathologic characteristics were analyzed. [score:1]
As shown in Figure 3A and 3B, transfection of miR-152 mimic significantly reduced B7-H1 mRNA levels in SGC-7901 and AGS cell lines. [score:1]
Relative luciferase activity in cells co -transfected with miR-152 or scramble control and a luciferase vector encoding luciferase gene fused wild type (WT) or mutant B7-H1 3′-UTR (B). [score:1]
Pearson's coefficient correlation was applied for analyzing associations between levels of miR-152 and mRNA levels of B7-H1, B7-1, B7-2 and B7-H3. [score:1]
As shown in Figure 6B, transfection of mimic of miR-152 significantly increased proliferation ability of T cells while scramble mimic control had no such effect. [score:1]
Clinicopathologic features of miR-152 in gastric cancer patients. [score:1]
As shown in Figure 2, there were no significant correlation between miR-152 and B7-H3, B7-1 and B7-2. However, there was marked correlation between miR-152 and B7-H1 (Figure 2A, P < 0.05, r = −0.51). [score:1]
Consistent with above result, the western blot and Flow Cytometry results showed that protein level of B7-H1 also markedly reduced after transfection with miR-152 mimic. [score:1]
Thus they were chosen for further functional analyses on miR-152. [score:1]
[#] P < 0.05 versus the miR-152 mimic+Inh con group. [score:1]
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[+] score: 238
The miRanda v3.0 target scanning algorithm predicts two target regions (Target-A and –C) for miR-128 and two target regions (Target-A, and -B) for miR-152 in the 2,172nt CSF-1 mRNA 3’UTR (Figure 3A). [score:11]
In contrast, expression of miR-152 appears to be positively correlated with CSF-1 expression, with miR-152 expressed at a high level in Hey and S KOV3 with lower expression seen in Bix3 cells and minimal expression in NOSE. [score:11]
In this report, we study 3’UTR targets for binding miRNAs, and find that both miR-128 and miR-152 down-regulate CSF-1 expression in ovarian cancer. [score:8]
To address this issue, we decided to study, in more detail, the roles of miR-128 (as being inversely correlated to CSF-1 expression) and miR-152 (as appearing to be most positively correlated to CSF-1 expression) in the post-transcriptional regulation of CSF-1 expression. [score:8]
The major CSF-1 mRNA 3’UTR contains a common miRNA target which is involved in post-transcriptional regulation of CSF-1. Our results provide the evidence for a mechanism by which miR-128 and miR-152 down-regulate CSF-1, an important regulator of ovarian cancer. [score:8]
Target-A appears to be a miRNA ‘hot-spot’ as our bioinformatics analysis predicted at least fourteen miRNAs, including miR-128 and miR-152, targeting a region of 2573–2577 (Target-A) in CSF-1 mRNA 3’UTR (Figure 3). [score:7]
To further confirm Target-A as an actual miRNA-responding sequence, miR-128 or miR-152 was overexpressed together with either wild type construct (Luc-CSF-1 3’UTR-Wt) or Target-A mutant construct (Luc-CSF-1 3’UTR-Mut). [score:7]
To determine the effects of miR-128 and miR-152 on the expression of CSF-1, either miR-128 or miR-152 were over-expressed or inhibited in S KOV3 and Bix3 ovarian cancer cells. [score:7]
This suggests that Target-A is a critical cis-acting regulatory sequence, and we have validated that it serves as a direct target for at least miR-128 and miR-152 (Figure 4). [score:7]
miR-128 and miR-152 down-regulate CSF-1 mRNA and protein expression. [score:6]
Target-A mutation also abrogated response of reporter RNA and activity to miR-128 and miR-152 over -expression (Figure 4). [score:6]
By using in silico text-mining algorithms against the CSF-1 mRNA 3’UTR, we selected miR-128 and miR-152 that would fit the profile of having regulatory abilities of CSF-1. While miR-128 and miR-152 possess target sequences in the CSF-1 mRNA 3’UTR, their expression patterns in the ovarian cancer cell lines proved to be different. [score:6]
Comparison of Figures 4B and 4D, however, demonstrate that the Target-A mutation construct largely attenuates the effect of miR-152 overexpression on luciferase activity. [score:6]
By mutations in putative miRNA targets in CSF-1 mRNA 3’UTR, we identified a common target for both miR-128 and miR-152. [score:6]
Either miR-128 or miR-152 was overexpressed together with either A, B) wild type construct (Luc-CSF-1 3’UTR-Wt) or C, D) Target-A mutant construct (Luc-CSF-1 3’UTR-Mut) in Bix3 cells. [score:5]
HHW and CFL carried out most of the experiments including the quantitative real-time qRT-PCR for CSF-1 mRNA, miR-128 and miR-152 as well as the overexpression and suppression of miRNAs and wrote the manuscript. [score:5]
In both cases, expressions of miR-128 and miR-152 follow their host gene expression patterns (Figure 2C, D). [score:5]
It was also recently revealed that both miR-128 and miR-152 have the ability to inhibit neuroblastoma cell motility and invasiveness when overexpressed [39]. [score:5]
Figure 4 Target-A is an active target for miR-128 and miR-152. [score:5]
Figure 5 miR-128 and miR-152 inhibit CSF-1 expression in S KOV3 and Bix3 cells. [score:5]
Either overexpression or inhibition of miR-152 has effect on both CSF-1 mRNA and protein levels. [score:5]
Furthermore, overexpression of miR-128 or miR-152 in Hey cells inhibited cell adhesiveness by 15-20% (p < 0.001) (Figure 6B). [score:5]
Either S KOV3 or Bix3 cells were transfected with the A, D) miR-128 or miR-152 overexpression plasmids (miR-128OE, miR-152OE); or B, E) inhibitor plasmids (miR-128Inh, miR-152Inh); or vector controls. [score:5]
After transfection with, miR-128 overexpression construct (miR-128OE), miR-152 overexpression construct (miR-152OE), or Empty vector (pCMV-miR), Hey cells were plated on A) an 8 micron pore membrane for a 6 hour directed motility assay. [score:5]
In this report, we add the findings that over -expression of miR-128 or miR-152 in ovarian cancer cells results in a significant reduction in both motility and adhesiveness (Figure 6), therefore inhibiting important aspects of invasiveness and metastasis. [score:5]
Our findings demonstrate that both miR-128 and miR-152 can negatively impact cell motility and adhesiveness of human ovarian cancer cells, important aspects of their metastatic potential, correlated with suppression of CSF-1 expression. [score:5]
In contrast, overexpression of either miR-128 or miR-152 in Bix3 cells transfected with the Target-A mutant construct did not decrease luciferase RNA significantly (p = NS) compared to the wild type construct (Figure 4C). [score:4]
The current study identifies miR-128 and miR-152 as important regulators for CSF-1 mRNA and protein expression, and of ovarian cancer cell behavior. [score:4]
To further confirm the expression pattern of miR-128 and miR-152 in ovarian cancer cells, we applied the Splinted Ligation technique to directly detect these miRNAs [34]. [score:4]
CSF-1 mRNA 3’UTR is a direct target for miR-128 and miR-152 in ovarian cancer cells. [score:4]
In CSF-1 mRNA 3’UTR, we identified three potential miRNA target sequences for miR-128 and/or miR-152 (Figure 3). [score:3]
In S KOV3, inhibition of miR-152 increased CSF-1 mRNA level by 1.42-fold (p < 0.001) (Figure 5B) and protein level by 9.43-fold (Figure 5C). [score:3]
In contrast, inhibition of miR-152 increased CSF-1 mRNA level by 3.32-fold (p < 0.001) (Figure 5E) and CSF-1 protein level (~60 kDa) by 1.22-fold (Figure 5F). [score:3]
In Bix3, overexpression of miR-152 decreased CSF-1 mRNA level by 61% (p < 0.001) (Figure 5D) and protein levels by 64% (Figure 5F). [score:3]
There was a small but statistically significant (p = 0.03) decrease in luciferase activity by miR-152 overexpression (Figure 4D). [score:3]
Expression of miR-128, miR-152, miR-27a, miR-214, and miR-454 in ovarian cancer cells. [score:3]
In S KOV3, overexpression of miR-152 decreased CSF-1 mRNA level by 86% (p < 0.001) (Figure 5A) and CSF-1 protein levels (~60 kDa) by 73% (Figure 5C). [score:3]
To find the actual target sequence for miR-128 and miR-152, we used a luciferase reporter system. [score:3]
Overexpression of either miR-128 or miR-152 in Bix3 cells co -transfected with the wild type construct decreased luciferase RNA by 39% and 93%, respectively (p < 0.001). [score:3]
Figure 6 Ovarian cancer cell adhesiveness and motility is inhibited by miR-128 and miR-152. [score:3]
The motility of Hey cells was significantly curtailed by over 50% by the overexpression of either miR-128 or miR-152 (p < 0.001) (Figure 6A). [score:3]
There was a small effect by overexpression of miR-152 on viability (p = 0.004) (Figure 6C). [score:3]
miR-152 and its host gene COPZ2 are silenced in tumor cells and introduction of miR-152 precursor inhibited tumor cell (MDA-MB-231, HeLa) growth [40]. [score:3]
miR-128 and miR-152 inhibit cellular motility and adhesion of ovarian cancer cells. [score:3]
Luciferase activity was decreased by 40% in response to miR-152 overexpression (p = 0.006) (Figure 4A,B). [score:3]
Recently, both miR-128 and miR-152 have been shown to inhibit neuroblastoma invasiveness [39]. [score:3]
In our study, both miR-128 and miR-152 reside in introns of R3HDM1 gene and COPZ2 gene, respectively. [score:1]
In contrast, miR-152 RNA is detected in Hey and S KOV3 cells, and not detectable in NOSE. [score:1]
miR-152 belongs to the miR-148 family whose putative role is still elusive, but it has been studied in hepatic [37], cervical [38], and brain cancers [39]. [score:1]
miR-152 RNA is detected in both Hey and S KOV3 cells. [score:1]
In contrast, miR-152 level was lower in the Bix3 cells than in the Hey and S KOV3 ovarian cancer cells (Figure 1D). [score:1]
These data suggest important biologic roles of miR-128 and miR-152 in cancer. [score:1]
In S KOV3, effects of either miR-128 or miR-152 are more prominent on CSF-1 protein level than on the CSF-1 mRNA level (Figure 5A-C). [score:1]
miR-152 gene is imbedded in the intronic region of COPZ2 gene, which is a subunit of coatomer protein complex 1 (COP1) known to be responsible for Golgi to ER transport [40]. [score:1]
Selected miRNAs for further analysis in this report are miR-152, -128, -27a, -214, -454; with results concerning the role of miR-130a and miR-301a in another context to be reported elsewhere (Woo et al. unpublished). [score:1]
B) of miR-152 in ovarian cancer cells. [score:1]
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4
[+] score: 175
Other miRNAs from this paper: hsa-mir-29a, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-185, hsa-mir-29c
These data indicated that miR-152-3p inhibited the expression of DNMT1, which led to upregulated expression of NF2 via demethylation. [score:10]
We also postulate that overexpression of miR-152-3p significantly enhances demethylation, which further upregulates the expression of NF2. [score:8]
Functionally, miR-152-3p overexpression, DNMT1 knockdown and NF2 overexpression significantly induced glioma cell apoptosis and inhibited their invasion. [score:8]
These results indicated that DNMT1 was a direct target of miR-152-3p, the expression of which might affect the biological function of the target. [score:8]
NF2 and miR-152-3p were down-regulated, DNMT1 was upregulated in GBM cell lines and tumour tissues. [score:7]
These data indicated that miR-152-3p might play an important role in GBM suppression via DNMT1 -mediated downregulation of NF2. [score:6]
Both knockdown of DNMT1 and overexpression miR-152-3p showed that demethylation activated the expression of NF2. [score:6]
DNMT1 knockdown and miR-152-3p overexpression induced cell apoptosis and inhibited cell invasion. [score:6]
Both miR-152-3p overexpression and DNMT1 knockdown significantly induced cell apoptosis and inhibited invasive activity. [score:6]
As shown in Fig. 5a, forced expression of miR-152-3p significantly decreasedDNMT1 mRNA expression. [score:5]
Overexpression of miR-152-3p and NF2 were achieved by transfecting the cells with miR-152-3p mimics (miR-152-3p) and NF2 -overexpressing vector obtained from Genepharma (Shanghai, China) and Vipotion (Guangzhou, China), respectively. [score:5]
In conclusion, our results suggest that miRNA-152-3p functions as a novel regulator to promote glioma cells invasion via DNMT1 -mediated downregulation of NF2 and can potentially be used as a treatment for GBM. [score:5]
Normal tissue and GBM were collected to determine mRNA expression of NF2 (a), DNMT1 (b) and miR-152-3p (c), as well as protein expression of NF2 and DNMT1 (d). [score:5]
MiR-152-3p increased the expression of NF2 through decreased DNMT1 expression. [score:4]
This is the first study to observe that miR-152-3p negatively regulates the expression of DNMT1 and invasiveness of GBM cells. [score:4]
MiR-152-3p was down-expressed in human malignancies, and served as a tumor suppressor. [score:4]
Methylation of NF2 and DNMT1 was markedly increased, and miR-152-3p was downregulated in GBM tissues and glioma cells. [score:4]
In the present study, we showed that miR-152-3p directly targeted DNMT1. [score:4]
Furthermore, miR-152-3p directly targeted DNMT1. [score:4]
As a result, mRNA expression of NF2 and miR-152-3p was significantly increased. [score:3]
c MiR-152-3p directly targets DNMT1. [score:3]
MiR-152-3p directly targeted DNMT1. [score:3]
MiR-152-3p, one of the two mature miR-152 sequences, shares the same seed sequence of approximately 6–7 nucleotides with the other members of miR-152 family; the aberrant expression of miR-152-3p was reported to be related to the pathogenesis of tumours such as hepatitis B virus-related hepatocellular carcinoma [13, 30]. [score:3]
a The viability of U251 cells was determined at 24, 48 and 72 h after miR-152-3p overexpression. [score:3]
mRNA expression of DNMT1, NF2, and miR-152-3p after transfection with miR-152-3p mimics, detected by RT-PCR in U251 cells (a). [score:3]
As a result, mRNA expression of NF2 and miR-152-3p were significantly increased. [score:3]
Fig. 1The expression of NF2, DNMT1, and miR-152-3p in GBM and malignant glioma cell lines. [score:3]
Protein expression of DNMT1 and NF2 was detected by Western blot after transfection with miR-152-3p mimics (b). [score:3]
Levels of mRNA expression of DNMT1, NF2, and miR-152-3p after transfection with DNMT1 siRNA and pcDNA-DNMT1 detected by RT-PCR in U251 cells (a). [score:3]
These results indicated that miR-152-3p can inhibit glioma cell proliferation and invasion activities by decreasing DNMT1. [score:3]
In order to confirm whether miR-152-3p was involved the expression of NF2, gain of function of miR-152-3p in U251 cells was performed. [score:3]
The expression of NF2, DNMT1 mRNA and miR-152-3p was determined with real-time quantification PCR. [score:3]
As expected, miR-152-3p overexpression significantly decreased cell viability compared with control treatment (Fig. 8a). [score:2]
These data indicated that NF2 might contribute to the development of GBM and that the process might be mediated by DNMT1 and miR-152-3p. [score:2]
Additionally, we observed that miR-152-3p overexpression significantly increased cell apoptosis and decreased the cell invasion compared with the control (Fig. 8b and c). [score:2]
a MiR-152-3p was predicted to target REST. [score:2]
However, the link between miR-152-3p, DNMT1 and methylation of NF2 in GBM is not clearly established. [score:1]
It was noted that miR-152-3p was significantly decreased in GBM (Fig. 1c). [score:1]
A dual luciferase system was used to confirm the relationship between miR-152-3p and DNMT1. [score:1]
Our results further demonstrate that DNMT1 and miR-152-3p form a negative feedback loop, while NF2 and miR-152-3p form a positive feedback loop. [score:1]
The siRNAs, miR-152-3p and their associated control were obtained from GenePharma, Shanghai, China. [score:1]
U251 cells, pretreated with pcDNA-NF2, DNMT1-siRNA or the miR-152-3p, were seeded at 5× 10 [5] cells/well in 6-well plates for 12 h. Subsequently, the cells were cultured with serum free medium for 12 h and then seeded at 2 × 10 [4] cells in 100 μl serum-free media per transwell coated with matrigel. [score:1]
Two psiCHECK2 luciferase plasmids containing DNMT1–3’UTR and DNMT1–3’UTR-MUT segments were transfected into HEK293 cells, respectively, together with miR-152-3p to confirm the correlation between mir-152-3p and DNMT1. [score:1]
Because miRNAs are wi dely accepted as a promising therapy for many diseases, especially tumours, miR-152-3p was investigated by RT-PCR in this study. [score:1]
Briefly, U251 cells transfected with pcDNA-NF2, DNMT1 siRNA, miR-152-3p, or their respective controls were exposed to 50 μM EdU for 2 h. After collection, the cells were fixed in 4% formaldehyde for about 20 min and then permeabilized with 0.5% Triton X-100 for about 10 min at RT. [score:1]
Subsequently, the effect of miR-152-3p on cell viability was determined. [score:1]
The restoration of miR-152-3p may have therapeutic application in the treatment of GBM. [score:1]
Glioblastomas NF2 DNMT1 miR-152-3p Demethylation Glioblastoma, also known as glioblastoma multiforme (GBM), is the most common and aggressive type of brain tumour in adults and accounts for about 69% of all gliomas [1, 2]. [score:1]
After miR-152-3p transfection, the methylation status of NF2 in U251 cells was determined with MSP (d) and bisulfite Sanger sequencing (e). [score:1]
At 48 h after miR-152-3p overexpression, cell apoptosis was evaluated by flow cytometry (b) and cell invasive activity was detected by transwell (c). [score:1]
miR-152 is one of the miRNAs that has attracted considerable interest in recent years, since it is implicated in glioma and other types of cancer [25, 26]. [score:1]
This study was conducted to detect the mechanism between miR-152-3p, DNMT1 and NF2 in GBM. [score:1]
It has been reported that mir-152-3p is significantly decreased in GBM. [score:1]
Alignment of the seed regions of miR-152-3p with DNMT1 3′ UTR are shown. [score:1]
Furthermore, it was noted that miR-152-3p resulted in the demethylation of NF2 gene (Fig. 5d and e). [score:1]
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[+] score: 148
These results suggest that miR-152 and miR-200b might play an essential role in gastric carcinogenesis and that HP infection may downregulate miR-152 and miR-200b expression resulting in a significant upregulation of B7-H1 expression in gastric cancer. [score:11]
Our data indicated that HP inhibited miR-152 and miR-200b expression in gastric cancer cells, and miR-152 and miR-200b target B7-H1 and suppress B7-H1 expression in gastric cancer cells. [score:11]
These results indicate that miR-152 and miR-200b indeed suppress B7-H1 expression in AGS cells, and support our conclusion that HP infection promotes B7-H1 expression through the downregulation of miR-152 and miR-200b in gastric cancer cells. [score:10]
The downregulation of miR-152 induces abnormal DNA methylation in HBV-related hepatocellular carcinoma (HCC) by inhibiting DNA methyltransferase 1 (DNMT1) expression [37]. [score:8]
Taken together, the findings of our study suggest that B7-H1 expression in gastric cancer cells can be upregulated by HP infection via the suppression of miR-152 and miR-200b. [score:8]
In contrast to transfection with the control nucleotides, transfection of the cells with miR-152 and miR-200b markedly inhibited B7-H1 expression, leading to only 21–22% of the cells expressing B7-H1 with IFN-γ treatment. [score:7]
We found that miR-152 and miR-200b expression levels were significantly decreased in HP-related gastric cancer and that miR-152 and miR-200b suppressed B7-H1 expression in gastric cancer cells. [score:7]
To determine whether the HP -induced increase in B7-H1 expression in human gastric cancer cells occurs via miRNAs targeting B7-H1, we studied two candidate B7-H1 miRNAs (miR-152 and miR-200b) that were predicted byTargetScan and PicTar in AGS cells after HP infection. [score:7]
MiR-152 and miR-200b target B7-H1 and suppress B7-H1 expression in gastric cancer cells. [score:7]
To confirm the regulation of B7-H1 expression by miR-152 and miR-200b, we investigated using a luciferase reporter system whether these miRNAs can bind to the 3' UTR of B7-H1 mRNA and inhibit its translation (Fig 5A). [score:6]
Many studies have indicated that miR-152 and miR-200b potentially function as tumor suppressors and are downregulated in various tumor types. [score:6]
These results further support our conclusion that HP infection promotes B7-H1 expression via the downregulation of miR-152 and miR-200b in human gastric cancer cells. [score:6]
In contrast, the treatment of the cells with inhibitors of miR-152 and miR-200b increased the expression of B7-H1 (Fig 4B). [score:5]
B7-H1 expression in AGS cells after treatment with mimics or inhibitors of miR-152 and miR-200b. [score:5]
These results suggest that HP infection may stimulate B7-H1 expression through the inhibition of miR-152 and miR-200b in gastric cancer cells. [score:5]
MiR-152 acts as a tumor suppressor that reduces the migratory and invasive capabilities of prostate cancer cells by targeting TGF-á [38]. [score:4]
It can be postulated that the hypermethylation of miRNA promoters caused by HP stimulating DNMT1 expression through the AKT-NFκB pathway may be the mechanism whereby HP downregulates miR-152 and miR-200b, which requires further investigation. [score:4]
Moreover, miR-152 is significantly reduced in ovarian cancer cells, and miR-152 regulates ovarian cancer cisplatin resistance by targeting DNMT1 [39]. [score:4]
Further studies should also determine the mechanisms by which HP infection decreases miR-152 and miR-200b expression and the role of miRNAs in host anti-HP immunity. [score:3]
However, this effect was markedly eliminated when inhibitors of miR-152 and miR-200b were transfected together. [score:3]
Thus, miR-152 and miR-200b function as important tumor suppressors in HP-related gastric cancer. [score:3]
In the miR-152 and miR-200b plus B7-H13’UTR groups, the luciferase activity was significantly inhibited. [score:3]
The 3′UTR of B7-H1 mRNA containing the miR-152 and miR-200b target sequences were cloned into the XhoI and NotI sites of psiCHECK-2 (Promega) using the primers B7-H1 3’UTR F1 and B7-H1 3’UTR R1 to generate a B7-H1 reporter. [score:2]
We determined the levels of miR-152 (Fig 6A) and miR-200b (Fig 6B) in 20 human gastric cancer samples using a qPCR assay and then analyzed their correlation to B7-H1 expression levels. [score:2]
Correlation between the B7-H1 -positive rate and miR-152 and miR-200b levels in human gastric cancer tissue samples. [score:1]
These results indicate that both miR-152 and miR-200b can bind to the 3’ UTR of B7-H1 mRNA (Fig 5B). [score:1]
Binding of miR-152 and miR-200b to B7-H1 mRNA. [score:1]
0168822.g006 Fig 6 The percentages of B7-H1 -positive cancer cells, as determined by double immunofluoresence, in 20 human gastric cancer samples were plotted against the levels of miR-152 (A) and miR-200b (B), as determined by qPCR. [score:1]
Levels of miR-152 and miR-200b in gastric cancer cells after HP infection or IFN-γ treatment. [score:1]
0168822.g005 Fig 5 (A) Schematic of B7-H1 mRNA showing potential miR-152 and miR-200b binding sites in the 3’-UTR and schematic of the luciferase reporter. [score:1]
To investigate the role of miR-152 and miR-200b in the elevation of B7-H1 expression in AGS cells, we treated the IFN-γ -treated AGS cells with several miRNAs, including miR-152 and miR-200b, and then determined the level of B7-H1 on the surface of the treated cells using flow cytometry. [score:1]
We found that HP infection reduced both miR-152(Fig 3A) and miR-200b (Fig 3B). [score:1]
The complementary miR-152 and miR-200b binding sites in the B7-H1 3’ UTR were inserted downstream of a luciferase reporter. [score:1]
In the present study, we investigated the mechanism whereby HP promotes B7-H1 expression through miR-152 and miR-200b. [score:1]
The percentages of B7-H1 -positive cancer cells, as determined by double immunofluoresence, in 20 human gastric cancer samples were plotted against the levels of miR-152 (A) and miR-200b (B), as determined by qPCR. [score:1]
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[+] score: 147
Other miRNAs from this paper: hsa-mir-140, hsa-mir-206, hsa-mir-331
On the other hand, overexpression of miR-152-3p suppressed HOTAIR expression, and the correlation between HOTAIR expression and miR-152-3p levels in melanoma tissues was negative. [score:9]
We also found that miR-152-3p up-regulation led to a decrease in the expression of endogenous c-MET mRNA and protein levels (Figure 5K and 5L), and the downstream PI3k/Akt/mTOR signaling pathway (Figure 5L). [score:6]
Accumulating evidence has shown that miR-152-3p is downregulated and functions as a tumor suppressor in many human tumors, including melanoma [41]. [score:6]
We also demonstrated that miR-152-3p functions as a tumor suppressor in melanoma by targeting c-MET. [score:5]
This inhibition and the effect of HOTAIR on melanoma cells can be reversed by co-transfection of miR-152-3p inhibitor. [score:5]
However, this inhibition was attenuated by co-transfection of miR-152-3p inhibitor (Figure 6B and 6C). [score:5]
Overexpression of miR-152-3p suppressed the proliferation and the invasive and migratory abilities of melanoma cells (Figure 5C–5H). [score:5]
The sponging of miR-152-3p by HOTAIR resulted in the loss of miR-152-3p suppression on the downstream target c-MET. [score:5]
miR-152-3p showed the highest upregulation after silencing HOTAIR in melanoma cells (Figure 3A). [score:4]
Because HOTAIR shares regulatory miR-152-3p with its target c-MET (Figures 4A and 5I), we further investigated whether HOTAIR acts as a sponge of miR-152-3p and promotes c-MET expression in melanoma cells. [score:4]
HOTAIR oncogenic activity functions in part through negative regulation of miR-152-3p in vivoTo further test the function of HOTAIR in vivo, we established a melanoma xenograft mo del by subcutaneously injecting A375 cells stably expressing control shRNA or shRNA-HOTAIR (Figure 7A). [score:4]
Dual luciferase reporter assays revealed that HOTAIR knockdown decreased the luciferase activity of pMIR-c-MET-WT, and the luciferase activity was rescued by miR-152-3p inhibitor in melanoma cells (Figure 6A). [score:3]
Furthermore, we detected the expression of miR-152-3p in melanoma tissues. [score:3]
miR-152-3p has been identified as a tumor suppressor gene in many human malignant tumors [31, 32]. [score:3]
This suggests that c-MET is a potential target of miR-152-3p. [score:3]
The 3’-untranslated region (3’-UTR) fragment of c-MET containing the putative binding sequences of miR-152-3p were cloned into pMIR-REPORT vectors, and the fragment of HOTAIR including the binding site was inserted into pMIR-REPORT vectors. [score:3]
As mentioned above, miR-152-3p expression was markedly decreased in melanoma (Figure 3C). [score:3]
The heat map data of sixty malignant melanoma tissues revealed the negative correlation between miR-152-3p and HOTAIR expression, and the Pearson correlation of HOTAIR and miR-152-3p levels was negative (Figure 3C and 3D). [score:3]
HOTAIR promotes the growth and metastasis of melanoma cells by sponging miR-152-3p, functionally releasing c-MET mRNA transcripts targeted by miR-152-3p, and activating the downstream PI3k/Akt/mTOR signaling pathway. [score:3]
Importantly, the effect of si-HOTAIR on the proliferation, migration and invasion of melanoma cells was rescued by the miR-152-3p inhibitor (Figure 6D–6I). [score:3]
We also demonstrated that c-MET is a functional target of miR-152-3p. [score:3]
miR-152-3p was downregulated in melanoma tissues compared to adjacent normal tissues (Figure 3B). [score:3]
Total proteins and RNA were extracted from tissues, the expression of HOTAIR, miR-152-3p and c-MET were detected using western blot or qRT-PCR. [score:3]
Overall, we demonstrated that c-MET is a functional target of miR-152-3p in melanoma. [score:3]
Figure 3 (A) The expression levels of miR-152-3p in A375 and A875 cells following transfection with si-HOTAIR or NC. [score:3]
miR-152-3p represses melanoma cells proliferation, invasion and migration by targeting c-MET. [score:3]
Figure 5 (A) The miR-152-3p expression profile in human melanoma cell lines (A375, A875, SK-MEL-1, SK-MEL-5 and SK-MEL-28) and human epidermal melanocytes (HEMa-LP and HEMn-LP). [score:3]
miR-152-3p was largely reduced in melanoma and suppressed the proliferation, invasion and migration of melanoma cells. [score:3]
c-MET is the functional target of miR-152-3p that affect proliferation, invasion and migration abilities of melanoma cells. [score:3]
We also detected the expression of miR-152-3p in human melanoma cell lines and human epidermal melanocytes. [score:3]
The miRNAs predicted were measured by qRT-PCR after silencing HOTAIR in melanoma cells, and the results showed that miR-152-3p had the highest upregulation. [score:2]
We constructed luciferase reporter plasmids containing the wild-type HOTAIR (pMIR-HOTAIR-WT) and mutant HOTAIR with mutations in the predicted miR-152-3p binding sites (pMIR-HOTAIR-MUT). [score:2]
HOTAIR directly binds to miR-152-3p. [score:2]
Dual luciferase reporter assays showed that over -expression of miR-152-3p led to a marked decrease in luciferase activity of the pMIR-c-MET-WT plasmid, while no significant changes were observed with the pMIR-c-MET-MUT plasmid in melanoma cells (Figure 5J). [score:2]
Lastly, we demonstrated that HOTAIR promotes melanoma growth and metastasis in vivo through negative regulation of miR-152-3p. [score:2]
HOTAIR oncogenic activity functions in part through negative regulation of miR-152-3p in vivo. [score:2]
In summary, these results suggest an important role for HOTAIR in modulating the c-MET pathway by competitively binding miR-152-3p in melanoma. [score:1]
These results reveal that HOTAIR promotes melanoma cell growth and metastasis by competitively binding miR-152-3p. [score:1]
RT-PCR showed that the miR-152-3p levels were increased in the shRNA-HOTAIR group (Figure 7D). [score:1]
To study the mechanism of action of miR-152-3p in melanoma cells, we found that the binding sites of miR-152-3p matched the 3’-UTR of c-MET according to miRanda (http://www. [score:1]
The miR-152-3p mimic was transfected into A375 and A875 cells to further study the function of miR-152-3p in melanoma cells (Figure 5B). [score:1]
Biotinylated miR-152-3p, biotinylated mutant miR-152-3p and biotinylated NC were synthesized by GenePharma (Shanghai, China), and were transfected into the melanoma cells using Lipofectamine 2000. [score:1]
The melanoma cells were co -transfected with hsa-miR-152-3p mimic and related reporter constructs. [score:1]
miR-152-3p was considerably lower in melanoma cells than in human epidermal melanocytes, especially in A375 and A875 cells (Figure 5A). [score:1]
The sequences were as follows: HOTAIR-small interfering RNA 1 (si-HOTAIR-1), 5′-GGAGAACACUUAAAUAAGUTT-3′; HOTAIR-small interfering RNA 2 (si-HOTAIR-2), 5′-AAAUCCAGAACCCUCUGACAUUUGC-3′; hsa-miR-152-3p mimic, 5′-UCAGUGCAUGACAGAACUUGG-3′; negative control (NC), 5′-UUCUCCGAACGUGUCACGUTT-3′. [score:1]
The potential miR-152-3p binding sites in HOTAIR transcripts were predicted using Starbase 2.0 (Figure 4A). [score:1]
HOTAIR was pulled down by biotin-labeled miR-152-3p oligos, but not the mutated oligos or biotinylated NC in melanoma cells (Figure 4E and 4F). [score:1]
Future studies to assess the role of the HOTAIR/miR-152-3p/c-MET axis in a clinical context are warranted. [score:1]
Moreover, a miR-152-3p mimic decreased HOTAIR levels in melanoma cells (Figure 3E). [score:1]
miR-152-3p promotes non-small cell lung cancer, colorectal cancer, and hepatocellular carcinoma cell growth and metastasis [31, 42, 43]. [score:1]
The effects of miR-152-3p on proliferation and the invasive and migratory abilities of melanoma cells were rescued by the c-MET plasmids (Figure 5C–5H, Figure 5K and L). [score:1]
To detect the levels of miR-152-3p, HOTAIR and c-MET, reverse transcription (RT) was conducted with Fermentas reverse transcription reagents and an Applied Biosystems [®] TaqMan [®] MicroRNA Reverse Transcription Kit (Applied Biosystems, CA). [score:1]
The Pearson correlation of c-MET and miR-152-3p levels was negative in 51 melanoma tissues from TCGA database (Supplementary Figure 1B). [score:1]
Furthermore, HOTAIR promoted the proliferation, invasion and migration of melanoma cells by acting as a ceRNA for miR-152-3p. [score:1]
HOTAIR acts as a ceRNA to promote melanoma cell growth and metastasis by sponging miR-152-3p. [score:1]
Figure 4 (A) The putative binding sites of miR-152-3p on the HOTAIR transcript, as predicted by starbase 2.0. [score:1]
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7
[+] score: 142
Other miRNAs from this paper: hsa-mir-222, hsa-mir-200b, hsa-mir-200c, hsa-mir-200a
In addition, miR-152 mimics induced a reduction in PVT1 expression, whereas miR-152 inhibitor caused an increase in PVT1 expression (Figure 6C). [score:7]
Previously, we demonstrated that DNMT1 is a direct target of miR-152 and miR-152 contributes to the hypomethylation of PTCH1 via inhibiting DNMT1 [8]. [score:6]
PVT1 enhances PTCH1 methylation via miR-152Previously, we demonstrated that DNMT1 is a direct target of miR-152 and miR-152 contributes to the hypomethylation of PTCH1 via inhibiting DNMT1 [8]. [score:6]
Collectively, PVT1 inhibits PTCH1 expression via competitively binding miR-152. [score:5]
Likewise, reduced α-SMA and collagen caused by siPVT1 were inhibited by miR-152 inhibitor (Figure 5E and Figure 5F). [score:5]
C. Relative gene expression of PVT1 was analyzed by in cells transfected with miR-152 mimics or inhibitor. [score:5]
Interestingly, miR-152 inhibitor reversed siPVT1 -suppressed HSC proliferation (Figure 5D). [score:5]
With the restoration of PTCH1 methylation, miR-152 inhibitor reversed siPVT1 -inhibited HSC activation. [score:5]
Interestingly, siPVT1 -induced PTCH1 demethylation was inhibited by miR-152 inhibitor. [score:5]
Taken together, PTCH1 expression is associated with its promoter methylation level and PVT1 contributes to HSC activation through regulation of miR-152 and PTCH1 methylation. [score:4]
Figure 7 PVT1 induces miR-152 down-regulation, PTCH1 methylation and activation of Hh pathway, then promotes EMT process, which contributes to the activation of HSCs. [score:4]
PVT1 induces miR-152 down-regulation, PTCH1 methylation and activation of Hh pathway, then promotes EMT process, which contributes to the activation of HSCs. [score:4]
Primary 2-day-old HSCs were transfected with siPVT1 for 48 h and then treated with miR-152 inhibitor for additional 48 h. The average percentage of DNA methylation was shown at the end of each row. [score:3]
D. Relative gene expression of pri-miR-152 was analyzed by in cells transfected with siPVT1. [score:3]
Notably, siPVT1 -induced PTCH1 was blocked down by miR-152 inhibitor (Figure 5E and Figure 5F). [score:3]
Our results showed that PVT1 enhanced PTCH1 methylation and caused a reduction in PTCH1 expression via competitively binding miR-152. [score:3]
In conclusion, we demonstrate that PVT1 can epigenetically inhibit PTCH1 via competitively binding miR-152, contributing to activation of Hh pathway and EMT process in liver fibrosis. [score:3]
Primary 2-day-old HSCs were transfected with siPVT1 for 48 h and then treated with miR-152 inhibitor for additional 48 h. The level of miR-152 was detected by in primary HSCs A. and CCl [4] mice B.. [score:3]
Our previous study showed that microRNA-152 (miR-152) inhibits liver fibrosis by attenuating DNA methyltransferase 1(DNMT1) -mediated PTCH1 methylation [8]. [score:3]
After transfection with siPVT1 and miR-152 inhibitor, HSCs were labelled with EdU for 12 h. HSC proliferative rate was detected using a Cell-Light™ EdU In Vitro Imaging Detection Kit (Guangzhou RiboBio Co. [score:3]
Bioinformatic analysis (RNA22) shows that PVT1 contains one target site for miR-152 (Figure 6A), indicating that there may be an interaction between miR-152 and PVT1. [score:3]
HSCs were transfected with siPVT1, siPVT1-2, miR-152 mimics or miR-152 inhibitor using Lipofectamine RNAiMAX at a final concentration of 10 nM. [score:3]
Consistent with these, the hypermethylation of PTCH1 was restored by miR-152 inhibitor in siPVT1 -transfected cells (Figure 4E). [score:3]
Figure 5Primary 2-day-old HSCs were transfected with siPVT1 for 48 h and then treated with miR-152 inhibitor for additional 48 h. The level of miR-152 was detected by in primary HSCs A. and CCl [4] mice B.. [score:3]
The results suggest that PVT1 is a target of miR-152. [score:3]
In addition, PVT1 inhibits miR-152 in a post-transcriptional manner. [score:3]
miR-152 level may be negatively correlated with PVT1 expression in liver fibrosis. [score:3]
miR-152 mimics and miR-152 inhibitor were additionally synthesized by GenePharma. [score:3]
Notably, all the effects of siPVT1 on HSC activation can be blocked down by miR-152 inhibitor. [score:3]
As shown in Figure 6E and Figure 6F, Bio-miR-152-Wt pulled down PVT1 while Bio-miR-152-Mut had no effect on PVT1, indicating a direct interaction between miR-152 and PVT1. [score:2]
To detect miR-152 and pri-miR-152 expressions, the RT reactions were performed using the TaqMan MicroRNA Assays (Applied Biosystems, Foster City, CA) according to the manufacturer's instructions. [score:2]
Interestingly, pri-miR-152 level was not affected by siPVT1 (Figure 6D), suggesting that PVT1 regulates miR-152 at the post-transcriptional level. [score:2]
PVT1 for miR-152 forward, 5′- TGCTGTTACCTGTATGCC-3′ and reverse, 5′-GCTTCATTACTTAATAAAGC-3′. [score:1]
Our data suggest that PVT1 may modulate PTCH1 methylation via miR-152. [score:1]
A. Schematic diagram of the miR-152 binding site in the PVT1 based on RNA22 software. [score:1]
Then, pmirGLO construct was used to generate a PVT1 luciferase reporter containing the miR-152 -binding sites (pmirGLO-PVT1-Wt) or mutated sites (pmirGLO-PVT1-Mut) (Figure 6A). [score:1]
We also identify PVT1/miR-152/PTCH1 as a new signaling network in liver fibrosis (Figure 7). [score:1]
Briefly, after 48 h of HSCs transfected with Bio-miR-152-wt, Bio-miR-152-mut, or Bio-miR-NC, the cells were washed with PBS followed by incubation in a lysis buffer for 10 min. [score:1]
To further determine the direct interaction between miR-152 and PVT1, biotinylated miR-152 (Bio-miR-152) pull-down assay was performed to confirm whether miR-152 could pull down PVT1. [score:1]
PVT1 enhances PTCH1 methylation via miR-152. [score:1]
E. Schematic diagram of wild type and the mutated form of miR-152 sequence. [score:1]
All the data above suggest that PVT1 can function as a ceRNA for miR-152. [score:1]
miR-152 is involved in the effects of PVT1 on HSC activation. [score:1]
B. Relative luciferase activities of luciferase reporters harboring the wild-type or mutant PVT1 were analyzed 48 h following transfection with the miR-152 mimics or miR-NC. [score:1]
miR-152 level was decreased by 79% at day 10 relative to day 2 (Figure 5A). [score:1]
Similarly, miR-152 level was reduced in CCl [4] group (Figure 5B). [score:1]
Figure 6 A. Schematic diagram of the miR-152 binding site in the PVT1 based on RNA22 software. [score:1]
F. Pull down assay to validate the direct interaction between PVT1 and miR-152. [score:1]
Our results indicated that miR-152 was responsible for the effects of PVT1 on PTCH1 methylation, which was consistent with our previous study [8]. [score:1]
Our results demonstrated that miR-152 mimics led to the reduction of luciferase activity of pmirGLO-PVT1-Wt in primary HSCs without affecting that of pmirGLO-PVT1-Mut (Figure 6B). [score:1]
Loss of PVT1 resulted in the elevation of miR-152 level (Figure 5C). [score:1]
We firstly detected miR-152 level in primary HSCs during culture days. [score:1]
Interaction between PVT1 and miR-152. [score:1]
Further studies were performed to examine the role of miR-152 in the effect of siPVT1 on HSC activation. [score:1]
The correlation between miR-152 and PVT1 was further determined in cells transfected with siPVT1. [score:1]
Luciferase reporter plasmids plus miR-152 mimics or miR-NC were co -transfected into 293T using Lipofectamine RNAiMAX. [score:1]
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8
[+] score: 133
Another important finding of this study is that an inhibition of TFRC expression by enforced up-regulation of miR-152 in human HepG2 cells was associated with a reduction of the level of intracellular iron and tumorigenic potential of the miR-152 -transfected HepG2 cells. [score:8]
D. Ectopic up-regulation of miR-152 inhibited TFRC expression and reduced level of TFRC protein E. in HepG2 cells. [score:8]
A luciferase miRNA 3′-UTR target vector carrying the predicted miR-152 binding site in the TFRC 3′-UTR, miRNA 3′-UTR target vector harboring two base mutations in the predicted miR-152 binding site in the TFRC 3′-UTR, and miRNA 3′-UTR target control vector were constructed and purchased from GeneCopoeia Inc. [score:8]
The results of the present study demonstrate that miR-152, in addition to miR-31, miR-210, and miR-320 miRNAs, targets TFRC directly, evidenced by functional miR-152-TFRC analyses and an inverse correlation between markedly decreased miR-152 level and TFRC up-regulation in human HCC cells and HCC tissue samples. [score:7]
Figure 4Regulation of TFRC expression by miR-152 A. The expression of miR-152 in human liver cancer cells. [score:6]
Mechanistically, the up-regulation of TFRC may be attributed to a markedly reduced expression of miR-152. [score:6]
Figure 5Expression of TFRC and miR-152 in human HCC samplesGene expression TFRC and miR-152, and clinical and tumor pathological data were extracted from TCGA. [score:5]
The expression of miR-152 in α-fetoprotein -positive PLC/PRF/5, Hep3B, and HepG2 cells was considerably lower than in α-fetoprotein -negative SK-HEP1 cells (Figure 4A) and inversely correlated with the expression of TFRC (Figure 4B). [score:5]
Furthermore, we demonstrated that the over -expression of TFRC was accompanied by and may be attributed mechanistically to a markedly reduced expression of microRNA-152 (miR-152) in HCC. [score:5]
C. Inhibition of TFRC expression in the 3′-UTR luciferase reporter assay after transfection of the SK-HEP1 cells with miR-152 or a negative control. [score:4]
This finding is in a good agreement with a previous report that showed down-regulation of miR-152 in human HBV-related HCC [46]. [score:4]
F. Effect of ectopic up-regulation of miR-152 in HepG2 on the level of intracellular iron and G. soft agar colony formation. [score:4]
Regulation of TFRC expression by miR-152. [score:4]
To test whether or not miR-152 directly targets TFRC, constructs retaining the core region of the TFRC 3′-UTR that harbors the putative binding site for miR-152 or mutated sequence in the miR-152 binding site were constructed and then co -transfected together with miR-152 into SK-HEP1 cells. [score:4]
The results of the present study showed an additional mechanism of the regulation of TFRC expression at post-transcriptional level mediated by miR-152, especially in full-fledged human HCC cells. [score:4]
Transfection with miR-152 efficiently down-regulated TFRC at both mRNA and protein levels (Figure 4D and 4E), while transfection with either miR-194 or miR-320 did not (data not shown). [score:4]
The expression levels of TFRC, miR-152, and miR-194 in human HCC tissue samples and normal liver samples were extracted from the TCGA database. [score:3]
Gene expression data for TFRC, miR-152, and miR-194, and clinical and tumor pathological data were extracted as. [score:3]
Gene expression TFRC and miR-152, and clinical and tumor pathological data were extracted from TCGA. [score:3]
Expression of TFRC and miR-152 in human HCC samples. [score:3]
In contrast, the level of miR-152 was markedly reduced in HCC tissue samples, with the values being significantly lower at each tumor stage of HCC progression, and inversely correlated with the TFRC expression (p = 0.0078). [score:3]
The results of in silico screening analysis demonstrated that several miRNAs, including miR-152, miR-194, and miR-320, could target the 3′-UTR of TFRC mRNA. [score:3]
Pearson product-moment correlation coefficients were used to determine the strength of association between levels of TFRC mRNA and the expression of miR-152. [score:3]
It has been reported previously that three miRNAs, miR-31, miR-210, and miR-320, in addition to miR-152, may target TFRC [43– 45]; however, considering a high degree of miRNA tissue specificity, the biological significance of any given miRNA-mRNA interaction should be evaluated in a specific target tissue context. [score:3]
B. Correlation plot of miR-152 and TFRC expression in human liver cancer cells. [score:3]
Expression of TFRC and miR-152 in human HCC. [score:3]
A. The expression of miR-152 in human liver cancer cells. [score:3]
In light of this, the results of the present study suggest that targeting of TFRC by miR-152 in HCC may be an attractive therapeutic approach for the treatment of HCC. [score:3]
Figure 4C shows that miR-152 efficiently suppressed luciferase activity by 22.3%. [score:3]
To confirm further the involvement of miR-152 in the regulation of TFRC at the post-transcriptional level, HepG2 cells were transfected with miR-152, miR-194, miR-320 microRNA mimics, or scrambled RNA oligonucleotide. [score:2]
To assess the direct interaction between miR-152 and the TFRC 3′-UTR, the luciferase constructs (1 μg) and the 80 nM of miR-152 mimic (Life Technologies) were co -transfected into SK-HEP1 cells, which were seeded in 6-well plates (1 × 10 [6] cells/transfection) using Lipofectamin™ 3000 transfection reagent (Life Technologies) following the manufacturer's recommendations. [score:2]
HepG2 cells (10 × 10 [3] cells), transfected with 20 nM of either miR-152 mimic or scrambled RNA oligonucleotide, were seeded onto 0.7% noble agar in growth media. [score:1]
HepG2 cells were seeded in 100 mm dishes at a density of 1 × 10 [6] cells/dish, and transfected with 20 nM of either miR-152, miR-194, or miR-320 microRNA mimics (Life Technologies), in three independent replicates, using Lipofectamin™ 2000 transfection reagent (Life Technologies) according to the manufacturer's instructions. [score:1]
In contrast, miR-152 did not affect luciferase activity in cells transfected with the TFRC 3′-UTR that harbored the mutated miR-152 binding site (data not shown). [score:1]
Additionally, transfection of HepG2 cells with miR-152 significantly reduced the level of intracellular iron (Figure 4F) and colony formation (Figure 4G). [score:1]
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9
[+] score: 114
In the aorta of the SD rats, we confirmed that the miR-152 expression was down-regulated in the HF-diet group, and it can be up-regulated after 12-week treatment of SHXXT (n = 6; Fig. 6C). [score:9]
To prove that miR-152 can regulate ERα gene expression via the suppression of DNMT1, we transfected the miR-152 precursor or inhibitor into the LPS -treated HASMCs. [score:8]
These findings indicate that miR-152 indirectly up-regulated ERα expression through its binding to DNMT1. [score:7]
On the contrary, DNMT1 protein levels were increased and consequently ERα protein levels were down-regulated by miR-152 inhibitor at 72 h (100 nM). [score:6]
The present study showed that miR-152 can down regulate DNMT1 which in turn inhibits methylation in the promoter of the ERα gene leading to higher ERα expression. [score:6]
To further examine whether miR-152 influences HASMC phenotypes through the change of ERα expression, the cell proliferation and migration were assessed at 48 h and 72 h after transfecting miR-152 precursor or inhibitor into the cells. [score:5]
The results showed that the DNMT1 protein levels were reduced and consequently ERα protein levels were up-regulated by miR-152 precursor at 72 h (100 nM; Fig. 7A). [score:4]
The reduced miR-152 can lose an inhibitory effect on DNA methyltransferase, which contributes to hypermethylation of the ERα gene. [score:3]
However, DNA methylation at ERα was increased by miR-152 inhibitor. [score:3]
The reduced microRNA-152 can lose an inhibitory effect on DNA methyltransferase, which leads to hypermethylation of the ERα gene and a decrease of ERα level. [score:3]
LPS -treated HASMCs were transfected with miR-152 precursor/inhibitor (25 nM and 100 nM) and a negative control miR (NC miR, 100 nM). [score:3]
Among 1,087 surveyed miRNAs, the expression level of miR-152 was decreased by 2.3-fold when HASMCs were treated with LPS for 24 h (data not shown). [score:3]
To examine the effect of miR-152 on cell proliferation, HASMCs were transfected with the miR-152 precursor or inhibitor and then were incubated in microplates at 37°C with 5% CO [2] for 48 h and 72 h. After that 0.5 mg/ml of dimethyl-thiazol- diphenyltetrazoliumbromide (MTT; Sigma-Aldrich, MO, USA) was added into each well. [score:3]
Therefore, we identified that miR-152 has an anti-atherosclerotic effect via its effect on the increase of ERα expression. [score:3]
0030635.g007 Figure 7LPS -treated HASMCs were transfected with miR-152 precursor/inhibitor (25 nM and 100 nM) and a negative control miR (NC miR, 100 nM). [score:3]
Expression of miR-152 in LPS -treated HASMCs and the aorta of the Sprague-Dawley rats. [score:3]
miR-152 expression in LPS -treated HASMCs. [score:3]
On the contrary, SHXXT could restore microRNA-152, decrease DNMT1 and increase ERα expression in both cellular and animal studies. [score:3]
Statin had no effect on microRNA-152, DNMT1 or ERα expression. [score:3]
Again, statin did not have any effect on increasing miR-152 but SHXXT could enhance miR-152 expression. [score:3]
Subsequent real-time PCR experiment confirmed that LPS can decrease miR-152 expression at 48 h and 72 h (P = 0.0015 and 0.006; Fig. 6A). [score:3]
Previous studies on cancers [23], [24] reported that miR-152 can bind to the 3′ untranslated region (UTR) of DNMT1. [score:3]
A negative control miRNA (#17110), hsa-miR-152 precursor (Product ID: PM12269) and hsa-miR-152 inhibitor (Product ID: AM12269) were purchased from the Ambion Inc. [score:3]
We validated that microRNA-152 can knock down DNMT1 in HASMCs leading to hypermethylation of the ERα gene. [score:2]
miR-152 regulates DNMT1 and ERα at the protein levels. [score:2]
microRNA-152 was found to be down regulated in the LPS -treated HASMCs. [score:2]
The DNMT family can be regulated by several miRs such as miR-29b, miR-148a and miR-152 [23]– [25], [27]. [score:2]
The results demonstrated that the transfected miR-152 precursor resulted in a concentration -dependent reduction of cell proliferation in the LPS -treated HASMCs at 48 h and 72 h (Fig. 7C; P<0.01). [score:1]
In conclusion, the present study showed that the level of miR-152 decreases under the pro-atherosclerotic stimulations. [score:1]
These results also suggested that miR-152 has an anti-atherosclerotic effect by decreasing cell proliferation. [score:1]
Gain and loss functions of ERα by miR-152. [score:1]
MSP analysis also showed that DNA methylation at ERα was reduced by miR-152 precursor in the LPS -treated cells (Fig. 7B). [score:1]
The effect of miR-152 on HASMC proliferation and migration. [score:1]
However, miR-152 did not influence HASMC migration at 48 or 72 h (data not shown). [score:1]
Accordingly, we speculated that miR-152 may be involved in DNMT1 -associated DNA methylation in the cardiovascular system. [score:1]
The present study showed that microRNA-152 decreases under the pro-atherosclerotic conditions. [score:1]
Furthermore, our cellular studies showed that miR-152 levels can be induced by SHXXT in a dose -dependent manner, but cannot be induced by simvastatin for 48 h or 72 h (Fig. 6B). [score:1]
0030635.g006 Figure 6(A) The miR-152 levels in the LPS -treated HASMCs were examined by real-time quantitative PCR and normalized to RU6B after 48 h and 72 h treatment with/without SHXXT. [score:1]
Therefore, we demonstrated a consistent change between DNMT1 and ERα methylation by the change of miR-152 levels. [score:1]
Unfortunately, we did have available human samples to compare miR-152 concentrations between atherosclerotic and non-atherosclerotic tissues. [score:1]
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10
[+] score: 111
Chronic exposure of these cells to 75 mM ethanol for five days resulted in a significant up-regulation of the expression of miR-7 and miR-144 and down-regulation of miR-203 and miR-15B with no significant change in the expression of miR-152 or miR-153 (Table 1). [score:11]
When cells were exposed to 75 mM ethanol for 5 days followed by a withdrawal period for 5 days, the expression of miR-7 and miR-15B was significantly down-regulated, the expression of miR-152 and miR-153 was unchanged and miR-203 was down-regulated to the extent that it could not be detected (Table 1). [score:11]
Chronic exposure of these cells to 75 mM ethanol for five days resulted in a significant down-regulation of the expression of miR-7, miR-15B and miR-152 with no change in the expression of miR-153. [score:8]
Chronic exposure of these cells to 75 mM ethanol for five days resulted in a significant down-regulation of the expression of miR-153 whereas the expression of miR-7, miR-152 and miR-15B was not significantly altered (Table 1). [score:8]
Specifically, miR-203, miR-144, miR-15B and miR-153 are all predicted to target the α1 isoform of the GABA [A] receptor, miR-7 and miR-153 are known to act co-operatively to regulate the expression of α-synuclein and miR-203, miR-144, miR-152, miR-7 and miR-15B are predicted to target isoforms of the 14-3-3 family. [score:8]
All four miRNAs were up-regulated in 1321 N1 cells following chronic ethanol exposure plus withdrawal whereas only miR-7, miR-152 and miR-15B were up-regulated in HEK293T cells. [score:7]
Similar to our findings, miR-152 was up-regulated by 2.74 fold following five days of chronic-intermittent ethanol exposure and five days of ethanol withdrawal but was not significantly up-regulated following ten days of chronic-intermittent exposure. [score:7]
The expression of miR-203 and miR-152 (~2 fold) was up-regulated following chronic-intermittent ethanol treatment and returned to near normal levels once ethanol was removed (Table 2). [score:6]
Interestingly, ethanol withdrawal resulted in an up-regulation of miR-7, miR-152, miR-203 and miR-15B similar to the expression changes seen in post mortem human brain [15]. [score:6]
Interestingly, ethanol withdrawal resulted in an up-regulation of miR-7, miR-152, miR-203 and miR-15B similar to the expression changes seen in post mortem human brain. [score:6]
Here we measured the expression of six miRNAs—miR-7, miR-153, miR-152, miR-15B, miR-203 and miR-144—which are predicted to target key genes involved in chronic alcoholism and other neurodegenerative disease. [score:5]
We measured the expression of six miRNAs—miR-7, miR-153, miR-152, miR-15B, miR-203 and miR-144—which are predicted to target key genes involved in chronic alcoholism and other neurodegenerative diseases. [score:5]
However, chronic ethanol exposure followed by withdrawal resulted in a significant up-regulation of miR-7, miR-153, miR-152 and miR-15B. [score:4]
We selected six miRNAs—miR-7, miR-152, miR-153, miR-144, miR-203 and miR-15B—which are predicted to target key genes involved in chronic alcoholism including GABA [A] receptors [18], α-synuclein [19], regulators of G protein signaling [20], and the 14-3-3 family of molecular chaperones [21]. [score:4]
Overall, exposure of these cells to chronic ethanol resulted in significant down-regulation of miR-7, miR-15B, miR-152 and miR-203 which persisted even after removal of ethanol. [score:4]
The expression of miR-152, miR-144, miR-15B and miR-153 did not change following either chronic-intermittent ethanol exposure or its removal (Table 2). [score:3]
Furthermore, the expression pattern of these four miRNAs was also significantly different between the three cell lines studied (MANOVA, Cell Line × Treatment Group, miR-7, F [2,8] = 9.92 P < 0.0001; miR-153, F [2,8] = 15.35 P < 0.0001; miR-152, F [2,8] = 10.62 P < 0.0001; miR-15B, F [2,8] = 14.58 P < 0.0001). [score:3]
MiR-7, miR-152, miR-153 and miR-15B were expressed in the 1321 N1 cell line whereas miR-144 and miR-203 were below the threshold for reliable detection. [score:3]
Only two of the six miRNAs measured in our study—miR-152 and miR-15B—were also differentially expressed in neuronal progenitor cells [17]. [score:1]
We measured the changes in expression of six miRNAs (miR-7, miR-153, miR-152, miR-144, miR-203 and miR-15B) in HEK293T cells, SH SY5Y neuroblastoma and 1321 N1 cells following ethanol treatment. [score:1]
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11
[+] score: 110
Other miRNAs from this paper: hsa-mir-181a-2, hsa-mir-181a-1, hsa-mir-191
The observed inverse correlation between miR-152 expression and its putative target strengthened the hypothesis of its direct regulation. [score:7]
In a previous study Yong Wang and colleagues showed, using microarray approach, that miR-152 is among the miRNAs more upregulated in replicative -induced fibroblast senescence [76] but it has never been studied to identify its targets and its role in the senescence process. [score:6]
Moreover miR-152 transfection in proliferating HDFn is followed by a significant decrease (about 50%, Figure 3E) of ITGA5 mRNA level and led to a strong down-regulation of itga5 protein level (Figure 3F) demonstrating that miR-152 was able to repress HDFn itga5 endogenous expression. [score:6]
The down-regulation of miR-152 putative target, was also possible confirmed at the protein level, in fact a western blot analysis showed a decrease of itga5 protein level in HDFn cells from p1 to p16 (Figure 3C). [score:6]
From an in silico prediction, by TargetScan 6.2 database, we selected ITGA5-3'UTR as putative target of miR-152. [score:5]
Analysis of miR-181A, and miR-152 target sites on COL16A1 and ITGA5 3'UTR were performed using the TargetScan 5.1 software available at http://www. [score:5]
Figure 3 (A) Predicted miR-152 target sites on human ITGA5 3'UTR were identified by TargetScan 6.2 software. [score:5]
We have identified ITGA5 as direct targets of miR-152. [score:4]
Overall, these findings suggest a mo del whereby during replicative senescence, a set of miRNAs, among them miR-152 and miR-181a, are upregulated, this sustain the senescent phenotype. [score:4]
Here, we have identified two miRNAs, miR-152 and miR-181a, upregulated in senescent human diploid fibroblasts. [score:4]
We confirmed, by real-time PCR that both, miR-152 and miR-181a, are significantly upregulated during fibroblasts replicative -induced senescence (Figure 1E). [score:4]
To confirm that ITGA5 mRNA is direct miR-152 target, we cloned ITGA53'UTR sequence, containing the miR-152 conserved binding site, downstream of a luciferase reporter gene. [score:4]
Several studies have identified specific sets of miRNAs up-regulated in keratinocytes and fibroblasts replicative senescence [75- 78], among these we focused on miR-152 and miR-181a. [score:4]
Integrins, beside transducing signals from the matrix to cells, bind to ECM to allow the fibroblasts to organize and remo del the matrix [81], this features is very limited in aged tissues and in particular in aged skin and this could be due in part to ITGA5 downregulation mediated by miR-152. [score:4]
To define the role of miR-152 and its molecular target ITGA5 in HDFn cell adhesion, we tested cell adhesion of proliferating HDFn over -expressing miR-152 compared to scrambled control. [score:4]
These results suggest that miR-152 and -181a overexpression, is sufficient per se to induce cellular senescence. [score:3]
In addition, we have shown that overexpression of miR-152 in fibroblasts significantly reduced cell adhesion, this finding indicate that ITGA5 might have a role in aged skin tissue. [score:3]
Overexpression of miR-152 and miR-181a had additional effects in HDFn cells, including the induction of the senescence markers p53 and p16INK4a(Figure 2B) and an increase in the number of cells positive for SA-β-galactosidase staining as shown by the images and blue cell quantification in Figure 2C and 2D. [score:3]
Although we do not exclude the possibility that other important senescence -associated miRNA-152 and miR-181a targets play a role in the senescent phenotype observed, we believe that the reduction in expression of ITGA5 and COL16A1 by miR-152 and miR-181a, strongly suggests that miRNAs have a complex role also in ECM remo deling typical of aged skin that deserve to be further investigated. [score:3]
miR-152 overexpression decreases ITGA5 protein levels; β-actin was used as a loading control. [score:3]
miR-152 represses ITGA5 expression and controls HDFn cell adhesion. [score:3]
These 3'UTR harbors at least one miR-152 target site that is highly conserved among vertebrates (Figure 3A). [score:3]
In addition, by in silico analyses we found that miR-152 and miR-181a, the latter involved in keratinocytes -induced senescence [75], have as putative targets many mRNA involved in cell adhesion and extracellular matrix remo delling, therefore we decide to study the role of these miRNAs in our experimental system. [score:3]
MiR-152, although has been detected in replicative -induced fibroblast senescence screenings [76], has never been studied to identify its targets and its role in the senescence process. [score:2]
The 3'-UTRs of miR-181a, and miR-152 target mRNAs were amplified by PCR from human genomic DNA using the following primer pairs: hCOL16A1-3'UTR-F 5'-GGCCTCTAGA CCCCACCTGCCTTTGGATG -3'; hCOL16A1-3'UTR-R 5'-GGCCTCTAGAGACTGAGTCTCATTA GTTGC -3'; hITGA5-3'UTR-F 5'-GGCCTCTAGAGT CCTCCCAATTTCAGACTC -3'; hITGA5-3'UTR-R 5'-GGCCTCTAGACTAGTTCTGGTCAGTGGGGG -3'. [score:2]
Here, we have investigated the role of miR-152 and miR-181a in replicative senescence of primary human dermal fibroblasts (HDFn) providing evidence that the expression of these miRNAs in young proliferating fibroblasts is sufficient to induce senescence markers. [score:1]
We found a decrease of about 20% in cells adhesion in miR-152 transfected cells as compared to control as shown in Figure 3G-H. These results suggested that miR-152 contribute to fibroblast adhesion in part by down regulation of ITGA5. [score:1]
To investigate the role of miR-152 and miR-181a in human dermal fibroblast, we set up overexpression by transfection with pre-miR-152, pre-miR-181a, or scrambled control sequence in proliferating HDFn cells. [score:1]
To investigate the role of miR-152 on ECM remo deling, we started a detailed analysis of its putative molecular targets. [score:1]
Ninety-six hours after transfection we observed a decrease about 40% in BrdU incorporation in the presence of miR-152 and miR-181a (respectively 18% and 19% versus 26% of scrambled control, Figure 1A) indicating a cell cycle G1-arrest. [score:1]
miR-152 and miR-181a induce senescence in human dermal fibroblasts. [score:1]
Figure 2 (A) 96 h after transfection of HDFn cells with scramble control (Ctr), miR-152 or miR-181a sequence, cells were subjected to a 4h BrdU-pulse, then collected, PI stained and analyzed by flow cytometry as described in Figure 1. (B) Western blot analysis of protein extract of HDFn transfected with miR-152 and miR-181a versus scramble control sequence (ctr). [score:1]
Human primary fibroblasts were transfected with human pre-miR 181a, pre-miR-152, and scramble sequence as negative control (Ambion, Texas, USA) using the Lipofecatmine RNAimax transfection reagent (Invitrogen) according to manufacturer protocols. [score:1]
miR-152 and miR-181a induce cellular senescence in HDFn cells. [score:1]
Relative luciferase activity, quantified 24 h after the transfection of reporter construct in presence of pre-miR-152, demonstrated that miR-152 repressed luciferase activity controlled by ITGA5 3-UTR (Figure 3D). [score:1]
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[+] score: 56
Other miRNAs from this paper: hsa-mir-148a, hsa-mir-148b, hsa-mir-489
j-l Data from MIRUMIR and miRpower showed that breast cancer patients with low expression of miR-148a, miR-148b or miR-152 had shorter survival time than those with high expression Our results showed the chemoresistant MCF-7/ADM cells exhibited lower miR-148a-3p, miR-148b-3p and miR-152-3p expression levels compared with chemosensitive MCF-7 cells (Fig.   4e). [score:6]
a-c Expression levels of miR-148a-3p, miR-148b-3p or miR-152-3p were inversely related with SPIN1 mRNA expression in MCF-7/ADM xenograft tumors (n = 20). [score:5]
f Expression of miR-148a-3p (r = − 0.7478, P = 0.0162), miR-148b-3p (r = − 0.6524, P = 0.0473) or miR-152-3p (r = − 0.8512, P = 0.0032) were inversely related with SPIN1 protein expression. [score:5]
Fig. 4miR-148a-3p, miR-148b-3p and miR-152-3p directly targeted SPIN1 and increased chemosensitivity in breast cancer cells. [score:4]
Notably, SPIN1 was identified as a direct target of the miR-148/152 family (miR-148a-3p, miR-148b-3p and miR-152-3p). [score:4]
MiR-152 inhibits tumor angiogenesis via targeting IGF-IR and IRS1 in breast cancer [41]. [score:4]
c-d The SPIN1 protein expression was clearly reduced after the transfection of miR-148a-3p, miR-148b-3p or miR-152-3p. [score:3]
e The expression levels of miR-148a-3p, miR-148b-3p and miR-152-3p were lower in MCF-7/ADM cells than that in MCF-7 cells. [score:3]
Here we found that miR-148-3p, miR-148b-3p and miR-152-3p were downregulated in Adriamycin-resistant MCF-7/ADM cells compared with the parental MCF-7 cells. [score:3]
Analysis on the xenograft tumors showed that expression of miR-148a-3p, miR-148b-3p or miR-152-3p was positively intercorrelated (Additional file 1: Figure S2). [score:3]
As shown in MIRUMIR [26, 32], low expression of miR-148b (P = 0.000377) or miR-152 (P = 0.0104) predicted poor survival of breast cancer patients (GEO database: GSE37405, n = 43). [score:3]
On the contrary, when the binding sites of these three miRNAs in the SPIN1 pmirGLO-3’UTR were mutated, its responsiveness to miR-148a-3p, miR-148b-3p or miR-152-3p regulation was abrogated (Fig.   4b). [score:2]
By luciferase assay, we observed a significant suppression of luciferase activity in cells transfected with miR-148a-3p, miR-148b-3p or miR-152-3p (Fig.   4a-b). [score:2]
Of the candidates, the miR-148/152 family (miR-148a-3p, miR-148b-3p and miR-152-3p), was of particular interest in light of its reported roles in regulating drug sensitivity of cancer cells [28– 30]. [score:2]
Transfection of miR-148a-3p, miR-148b-3p or miR-152-3p resulted in a significant decrease in survival of MCF-7/ADM and MCF-7 cells in Adriamycin-added medium (Fig.   4f-i). [score:1]
Moreover, a microarray analysis by Kovalchuk et al. found that two members (miR-148a and miR-152) of the family displayed more than 370-fold decreases in MCF-7/ADM cells versus MCF-7 cells [31], further indicating their possible involvement in breast cancer chemoresistance. [score:1]
a The 3’-UTR element of SPIN1 mRNA is partially complementary to miR-148a-3p, miR-148b-3p and miR-152-3p. [score:1]
As expected, miR-148a-3p, miR-148b-3p or miR-152-3p could increase Adriamycin sensitivity in breast cancer cells in vitro. [score:1]
f-g Transfection of miR-148a-3p, miR-148b-3p, miR-152-3p, or cotransfection of these three miRNAs significantly increased the miRNAs levels. [score:1]
The pmirGLO vector (Promega) was used to construct the recombinant plasmid pmirGLO- SPIN1 containing the SPIN1 mRNA 3’-UTR fragments which possess binding sites of miR-148a-3p, miR-148b-3p and miR-152-3p [11]. [score:1]
h-i miR-148a-3p, miR-148b-3p and miR-152-3p decreased Adriamycin resistance in MCF-7/ADM and MCF-7 cells. [score:1]
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[+] score: 40
In addition to miR-150 which was the miRNA with most significant gender differences in expression, we observed similar associations for mir-138 and mir-34a where differences in expression levels between males and females were significant (p = 0.002 and p = 0.04, respectively) when data was normalized to a combination of mir-152 and mir-23b, but not when RNU6B or U6 were used for normalization. [score:5]
Although we identified mir-152 and mir-23b miRNAs as most stable and appropriate endogenous controls for normalizing expression of hepatic miRNAs involved in regulation of drug metabolizing genes, the relevance and applicability of these findings to other disease conditions/tissue types should be systematically evaluated before making a decision on the choice of appropriate endogenous controls. [score:4]
However, normalization to a combination of mir-152 and mir-23b allowed us to discriminate more accurately between the microRNA relationships and identified mir-10a as the only microRNA with high correlation to mir-10b expression. [score:3]
To further study the impact of normalizer variability on relative quantitation of microRNA levels, we studied the correlations between mir-10b expression levels and other microRNAs when the data was normalized to U6, RNU6B or a combination of mir-152 and mir-23b. [score:3]
Gender differences (Males > Females) are observed in mir-150 expression when data is normalized to a combination of mir-152 and mir-23b (geometric mean) but this effect is lost when data is normalized to RNU6B or U6. [score:3]
Figure  4 shows the effect of normalization on mir-150 levels (mean expression in males vs females) when data is normalized to either U6 or RNU6B or a combination of mir-152 and mir-23b, the two most stable microRNAs. [score:3]
Significant gender differences (females < males) were observed in mir-150 expression when data was normalized to mir-152 and mir-23b, but when not data was normalized to U6. [score:3]
Normalization to a combination of mir-152 and mir-23b identified females as having a significantly lower mean mir-150 expression as compared to males. [score:2]
We also looked at the correlation between RQ values for mir-10b when the data was normalized to U6, RNU6B or a combination of mir-152 and mir-23b. [score:1]
An analysis using GeNormplus to identify the minimum number of endogenous controls required, identified this number as two, with the combination of mir-23b and mir-152 being the most stable. [score:1]
mir-152 and mir-23b were identified to be the two most stable candidates by both Normfinder and GeNormplus in our analysis, and were used as endogenous controls for normalization of hepatic miRNA levels. [score:1]
Along with U6 and RNU6B, the microRNAs analyzed as candidate endogenous controls included mir-152, mir-23b, mir-10a, mir-27a, mir-128a, mir-200a, mir-138 and mir-9. GeNormplus is integrated into Qbaseplus, which can be downloaded for a fully functional 15-day trial from Biogazelle (http://www. [score:1]
Both Normfinder and GeNormplus identified mir-152 and mir-23b as the two most stable candidates. [score:1]
There was also little to no correlation in the RQ results obtained when data was normalized to U6 and when it was normalized to a combination of mir-152 and mir-23b. [score:1]
As mir-23b is much more abundant than mir-152, it makes sense to take a geometric mean of both for data normalization. [score:1]
Similarly mir-152 was the most stable in Normfinder rankings and 2 [nd] most stable in GeNormplus rankings. [score:1]
There was little or no correlation in mir-10b levels between U6 and RNU6B normalized data (r = 0.149) or between U6 and mir-152/mir-23b normalized data (r = −0.192), with some correlation being observed between RNU6B and mir-152/mir-23b normalized data (r = 0.644). [score:1]
At the same time, normalizing to a combination of mir-152 and mir-23b also allowed us to identify a negative relationship between mir-10b and mir-27b. [score:1]
Normfinder analyses also identified mir-152 and mir-23b as the two most stable candidates. [score:1]
Normalizing the data to a combination of mir-152 and mir-23b however, identified only mir-10a as being highly associated with mir-10b while mir-27b was additionally identified as being negatively correlated to mir-10b. [score:1]
An analysis using GeNormplus to identify the required number of endogenous controls for our analysis identified this number to be two, with a combination of mir-23b and mir-152 identified as the most stable of the reference candidates (Figure  3B). [score:1]
An analysis of the best ranking candidates (RNU6B, mir-10a, mir-23b, mir-27b, mir-128a, and mir-152) using GeNormplus identified mir-23b as the most stable gene, followed by mir-152, mir-27b and mir-10a respectively (Figure  3A). [score:1]
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[+] score: 38
Moreover, experimental upregulation of miR-152 results in reduced KIT and MET mRNA as well as protein levels, down-regulates the PI3K/AKT-pathway, diminishes cellular growth and enhances apoptotic cell death [43]. [score:7]
Pazzaglia L. Novello C. Conti A. Serena P. Picci P. Benassi M. S. miR-152 down-regulation is associated with MET up-regulation in leiomyosarcoma and undifferentiated pleomorphic sarcomaCell. [score:7]
On the other hand, experimental upregulation of miR-152 reduces levels of MET and KIT in leiomyosarcoma cell lines [43]. [score:4]
In leiomyosarcoma, miR-152 is downregulated [43]. [score:4]
The downregulation of miR-152 in leiomyosarcoma is associated with increased KIT and MET-levels [43]. [score:4]
As with leiomyosarcoma, miR-152 is downregulated in UPS and negatively correlates with MET and KIT mRNA levels [43]. [score:4]
In leiomyosarcoma, miR-152 targets the tyrosine-protein kinases: MET and KIT [43]. [score:3]
miR-152 has several targets, such as DNA (cytosine-5)-methyltransferase-1 (DNMT1) in endometrial cancer and TNFRF6B in hepatocellular carcinoma. [score:3]
Kohler C. U. Bryk O. Meier S. Lang K. Rozynek P. Bruning T. Kafferlein H. U. Analyses in human urothelial cells identify methylation of miR-152, miR-200b and miR-10a genes as candidate bladder cancer biomarkersBiochem. [score:1]
Moreover, miR-152 diminishes proliferation and enhances apoptotic cell death, reduces the activity of the PI3K/AKT cascade and leads to S phase cell cycle arrest [43]. [score:1]
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[+] score: 37
In addition, miR-143 is frequently downregulated in CRC cells, where it normally targets DNMT3A (Ng et al., 2009), and downregulated expression of miR-152 in HBV-related HCC correlates with increased expression of DNMT1 (Huang et al., 2010). [score:13]
Similarly, DNMT1 is targeted by miR-148a and miR-152 in cholangiocarcinoma cells, and their ectopic expression suppresses DNMT1 and induces expression of the tumor suppressor genes Ras association domain family 1A (RASSF1A) and p16 (Braconi et al., 2010). [score:11]
Forced expression of miR-152 in liver cell lines reduces DNMT1 expression and global DNA methylation, whereas inhibition of miR-152 causes global DNA hypermethylation and increased methylation of the glutathione S-transferase pi 1 (GSTP1) and CDH1 promoter regions. [score:7]
Down-regulated microRNA-152 induces aberrant DNA methylation in hepatitis B virus-related hepatocellular carcinoma by targeting DNA methyltransferase 1. Hepatology 52 60– 70 10.1002/hep. [score:6]
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[+] score: 34
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-22, hsa-mir-29a, hsa-mir-30a, hsa-mir-29b-1, hsa-mir-29b-2, mmu-let-7g, mmu-let-7i, mmu-mir-1a-1, mmu-mir-29b-1, mmu-mir-30a, mmu-mir-127, mmu-mir-132, mmu-mir-133a-1, mmu-mir-136, mmu-mir-144, mmu-mir-146a, mmu-mir-152, mmu-mir-155, mmu-mir-10b, mmu-mir-185, mmu-mir-190a, mmu-mir-193a, mmu-mir-203, mmu-mir-206, hsa-mir-148a, mmu-mir-143, hsa-mir-10b, hsa-mir-34a, hsa-mir-203a, hsa-mir-215, mmu-mir-34c, mmu-mir-34b, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-132, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-143, hsa-mir-144, hsa-mir-127, hsa-mir-136, hsa-mir-146a, hsa-mir-185, hsa-mir-190a, hsa-mir-193a, hsa-mir-206, mmu-mir-148a, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-22, mmu-mir-29a, mmu-mir-29c, mmu-mir-34a, mmu-mir-337, hsa-mir-1-1, mmu-mir-1a-2, hsa-mir-155, mmu-mir-29b-2, hsa-mir-29c, hsa-mir-34b, hsa-mir-34c, hsa-mir-378a, mmu-mir-378a, hsa-mir-337, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, mmu-mir-215, mmu-mir-411, mmu-mir-434, hsa-mir-486-1, hsa-mir-146b, hsa-mir-193b, mmu-mir-486a, mmu-mir-540, hsa-mir-92b, hsa-mir-411, hsa-mir-378d-2, mmu-mir-146b, mmu-mir-193b, mmu-mir-92b, mmu-mir-872, mmu-mir-1b, mmu-mir-3071, mmu-mir-486b, hsa-mir-378b, hsa-mir-378c, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-378f, hsa-mir-378g, hsa-mir-378h, hsa-mir-378i, mmu-mir-378b, hsa-mir-203b, mmu-mir-3544, hsa-mir-378j, mmu-mir-133c, mmu-let-7j, mmu-mir-378c, mmu-mir-378d, mmu-let-7k, hsa-mir-486-2
Down-regulated miRNAs Up-regulated target genes mmu-mir-148a ARL6IP1, ARPP19, ATP2A2, CCNA2, CSF1, EGR2, ERLIN1, ERRFI1, FIGF, GADD45A, GMFB, ITGA5, KLF4, KLF6, LIMD2, MAFB, NFYA, PDIA3, PHIP, PPP1R10, PPP1R12A, PTPN14, RAI14, RSBN1L, SERPINE1, SIK1, SLC2A1, TMEM127, TMSB10, TMSB4X mmu-mir-411 APOLD1, SPRY4 mmu-mir-136 RYBP, ARL10, GLIPR2, UGGT1 Up-regulated miRNAs Down-regulated target genes mmu-mir-34a/c DAB2IP, DMWD, EVI5L, FAM107A, MAZ, SPEG, TFRC, TTC19 mmu-mir-92b COL1A2, DAB2IP, G3BP2, HOXC11, LBX1, NFIX, PKDCC, PRKAB2 mmu-mir-132 ACTR3B, AMD1, GPD2, HBEGF, KBTBD13, KCNJ12, PRRT2, SREBF1, TLN2 mmu-mir-146a IRAK1, TLN2 mmu-mir-152 EML2, GPCPD1, NFIX, RPH3AL, SH3KBP1, TFRC, TRAK1, UCP3 mmu-mir-155 DUSP7, G3BP2 mmu-mir-185 DAB2IP, FAM134C, SYNM, TMEM233 mmu-mir-203 APBB2, CACNG7, FKBP5, GDAP1, HBEGF, KCNC1, SIX5, TMEM182 mmu-mir-206 DMPK, G3BP2, GPD2, KCTD13, MKL1, SLC16A3, SPEG mmu-mir-215 KLHL23 Figure 5The network displays the predicted interactions between age-related miRNAs and mRNAs from the sequencing and was generated using Cytoscape (version 3.0, www. [score:17]
Down-regulated miRNAs Up-regulated target genes mmu-mir-148a ARL6IP1, ARPP19, ATP2A2, CCNA2, CSF1, EGR2, ERLIN1, ERRFI1, FIGF, GADD45A, GMFB, ITGA5, KLF4, KLF6, LIMD2, MAFB, NFYA, PDIA3, PHIP, PPP1R10, PPP1R12A, PTPN14, RAI14, RSBN1L, SERPINE1, SIK1, SLC2A1, TMEM127, TMSB10, TMSB4X mmu-mir-411 APOLD1, SPRY4 mmu-mir-136 RYBP, ARL10, GLIPR2, UGGT1 Up-regulated miRNAs Down-regulated target genes mmu-mir-34a/c DAB2IP, DMWD, EVI5L, FAM107A, MAZ, SPEG, TFRC, TTC19 mmu-mir-92b COL1A2, DAB2IP, G3BP2, HOXC11, LBX1, NFIX, PKDCC, PRKAB2 mmu-mir-132 ACTR3B, AMD1, GPD2, HBEGF, KBTBD13, KCNJ12, PRRT2, SREBF1, TLN2 mmu-mir-146a IRAK1, TLN2 mmu-mir-152 EML2, GPCPD1, NFIX, RPH3AL, SH3KBP1, TFRC, TRAK1, UCP3 mmu-mir-155 DUSP7, G3BP2 mmu-mir-185 DAB2IP, FAM134C, SYNM, TMEM233 mmu-mir-203 APBB2, CACNG7, FKBP5, GDAP1, HBEGF, KCNC1, SIX5, TMEM182 mmu-mir-206 DMPK, G3BP2, GPD2, KCTD13, MKL1, SLC16A3, SPEG mmu-mir-215 KLHL23 Figure 5The network displays the predicted interactions between age-related miRNAs and mRNAs from the sequencing and was generated using Cytoscape (version 3.0, www. [score:17]
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[+] score: 33
In addition, downregulation of miR-148b was found to associate with poorer outcomes in patients with hepatocellular carcinoma [21], and high miR-152 expression developed a negative impact on recrudescence in NSCLC [22]. [score:6]
The miR-148/152 family consists of three highly homologous members (miR-148a, miR-148b, and miR-152), of which ectopic expression was observed in multiple diseases such as: atherosclerosis, diabetes, and cancers [13– 15]. [score:5]
Results from subgroups suggested that miR-148a and miR-148b exerted enhanced OS/CSS, with a pooled HR of 0.76 (95% CI: 0.69-0.90) and 0.49 (95% CI: 0.39-0.61), while abnormal miR-152 expression developed no statistical impact (HR=0.40, 95% CI: 0.12-1.29; Figure 3A). [score:3]
In analysis of microRNA subgroups, our results demonstrated that miR-148a and miR-148b promoted favorable OS/CSS (HR=0.76, 95% CI: 0.69-0.90) and (HR=0.49, 95% CI: 0.39-0.61), nevertheless abnormal miR-152 expression exerted no statistical significance (HR=0.40, 95% CI: 0.12-1.29). [score:3]
Admittedly, miR-148a, miR-148b, and miR-152 are the three members of the miR-148/152 family with the same seed sequence, of which are pivotal for binding to target mRNAs. [score:3]
In addition, Wang et al detected the circulating miR-148a, miR-148b, and miR-152 and revealed that loss of miR-148a expression independently predicted a shorter overall time in patients with HCC than miR-148b and miR-152 [37]. [score:3]
In a breast cancer study, Xu et al that high DNMT1 expression was responsible for hypermethylation of miR-148a and miR-152 promoters. [score:3]
miR-148a, microRNA-148a; miR-148b, microRNA-148b; miR-152, microRNA-152. [score:1]
A literature search through online databases such as PubMed, Embase, and Web of Science were performed up to March 2017, using the following keywords (“microRNA-148a” or “miR-148a” or “microRNA-148b” or “miR-148b” or “microRNA-152” or “miR-152”) and (“cancer” or “carcinoma” or “Neoplasm” or “Tumor”) and (“prognostic” or “prognosis” or “survival” or “outcome” or “recurrence” or “relapse”). [score:1]
In addition, the deficiencies of studies focusing on miR-152 and cancer outcomes also accounted to some extent. [score:1]
Besides, miR-148a/b are promising biomarkers for predicting patients overall outcomes than miR-152. [score:1]
Currently, miR-148/152 family members include miR-148a, miR-148b, and miR-152, of which the three share a common seeds sequence in domains [31]. [score:1]
Furthermore, Wang et al reported the onceogenic value of miR-152 in colorectal carcinoma, but failed to demonstrate a significant impact on prognosis [24]. [score:1]
Diverse prognostic values between miR-148a/b and miR-152 may attributed to different domains of the three, even though they possessed the same seed sequence. [score:1]
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P-values are: miR-148a expression in 501mel  = 0.0940 and in MeWo  = 0.0148. miR-148b expression in 501mel  = 0.0023 and in MeWo  = 0.0065. miR-152 expression in 501mel  = 0.0054 and in MeWo =  0.9316. [score:7]
Expression of miR-152 in 501mel was 2.7 fold lower than in HEK293 cells and was much lower then the expression of miR-148a and miR-148b in all cell types (see Table 2). [score:5]
Similarly, miR-152 was shown to be downregulated in a highly invasive melanoma cell line (Mel Im) [30]. [score:4]
0011574.g006 Figure 6. Expression of endogenous miRNAs miR-148a, miR-148b and miR-152 in HEK293, 501mel and MeWo cells. [score:3]
It has not been shown previously that miR-148 and/or miR-152 can target Mitf. [score:3]
Expression of endogenous miRNAs miR-148a, miR-148b and miR-152 in HEK293, 501mel and MeWo cells. [score:3]
Similarly, hypermethylation of the miR-148, 124a3 and miR-152 genes was found in 34-86% of primary human breast cancer specimens [50]. [score:1]
miR-148 and miR-152. [score:1]
ND (1/9) ND (0/9) 34.69 (7/9) 37.39 (1/3) miR-124 34.37 (9/9) 34.73 (5/9) 35.09 (2/9) 32.68 (3/3) miR-506 35.19 (2/9) 34.73 (3/9) 32.87 (9/9) ND (0/9) miR-148a 27.90 (9/9) 28.29 (9/9) 28.82 (9/9) 33.12 (3/3) miR-148b 28.37 (9/9) 28.65 (9/9) 29.37 (9/9) 35.19 (1/3) miR-152 34.08 (9/9) 35.12 (9/9) 34.26 (9/9) 35.05 (2/3) miR-16 contr. [score:1]
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Among the other miRNAs expressed in association with Zr levels, we found that miR-152, miR-494 and miR-335 had hundreds of potentially regulated targets, demonstrating that they might have a relevant role in the context we are studying. [score:6]
As expected by the large number of predicted targets, miR-152, miR-335 and miR-494 resulted to share targets such as the cytokine receptor KIT, the Rho -dependent Protein Kinase (ROCK-1), proteins belonging to the tyrosine phosphatase family (PTPN11 and PTPN14) and proteins belonging to the Rho Guanine Nucleotide Exchange Factor (ARHGEF2, ARHGEF12 and ARHGEF17). [score:5]
The common targets we identified for miR-152, miR-494 and miR-335 seem to be largely involved in the regulation of inflammatory processes. [score:4]
In the present study on an obese population, we found that the exposure to Zr levels traced in hair is associated with a distinct signature of 7 miRNAs (miR-99b, miR-142-5p, miR-152, miR-193a-5p, miR-323-3p, miR-335, miR-494) expressed in peripheral blood. [score:3]
The seven miRNAs (miR-99b, miR-142-5p, miR-152, miR-193a-5p, miR-323-3p, miR-335, miR-494) associated with Zirconium levels with FDR P < 0.1, were selected for downstream target prediction analysis. [score:3]
Cellular location of targets shared by miR-152, miR-335 and miR-494. [score:3]
More specifically, we identified that miR-152, miR-494 and miR-335 had the largest number of potentially regulated mRNAs that were 254, 208 and 105 respectively. [score:2]
Seven miRNAs (miR-99b, miR-142-5p, miR-152, miR-193a-5p, miR-323-3p, miR-335, miR-494) resulted specifically associated with Zr levels. [score:1]
Using an FDR linear step-up adjustment for multiple comparisons (FDR P < 0.1), we found 7 miRNAs (miR-99b, miR-142-5p, miR-152, miR-193a-5p, miR-323-3p, miR-335, miR-494) specifically associated with Zr levels traced in the hair (Table 2). [score:1]
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miR-152 was specifically downregulated in arthritic rat mo del, enforced expression of miR-152 in FLS which resulted in a significantly downregulated DNMT1 expression, which in turn indirectly upregulated the SFRP4 expression and sequentially inhibited the canonical Wnt pathway activation, leading to a remarked decrease of FLS proliferation [77]. [score:19]
Among these, the miR-152 and miR-375 were downregulated, and the miR-663 was upregulated in RA patients or rat mo dels. [score:7]
Recently, a series of investigations conducted by Miao et al. demonstrated that several miRNAs, including miR-152, miR-375, and miR-663, were involved in the pathogenesis of RA by targeting Wnt signaling pathways [35, 74, 77, 78]. [score:1]
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Milk-derived DNMT -targeting exosomal miRNAs (miRNA-148a, miRNA-152, miRNA-21, miRNA-29s) may play a pivotal epigenetic role in reducing CpG methylation of critical gene regulatory sites of FTO resulting in increased FTO expression required for increased postnatal mRNA transcription (Figure 2) [135]. [score:6]
This in turn led to a decrease in global DNA methylation and increased the expression of two lactation-related genes, serine/threonine protein kinase AKT and peroxisome proliferator-activated receptor-γ (PPARG), whereas inhibition of miRNA-152 showed the opposite results. [score:5]
The expression of DNMT1 is inversely related to the expression miRNA-148a and miRNA-152 [119, 120]. [score:5]
The generation of DNMT -targeting miRNAs (miRNA-152, miRNA-148a, miRNA-29, miRNA-21) is thus a fundamental epigenetic mechanism increasing lactation-specific gene transcription thereby enhancing lactation performance as well as milk yield in domestic animals. [score:3]
The forced expression of miRNA-152 in dairy cow MECs resulted in a marked reduction of DNMT1 at both mRNA and protein levels. [score:3]
Wang et al. [116] found that the expression of miRNA-152 significantly increased during lactation in the mammary glands of dairy cows producing high quality milk compared with miRNA-152 levels in cows producing low quality milk. [score:2]
Furthermore, miRNA-152 enhanced the viability and multiplication capacity of dairy cow MECs [116]. [score:1]
miRNA-148a, miRNA-148b, and miRNA-152 are three members of the miRNA-148/152 family that share substantial homology in their seed sequence. [score:1]
[1 to 20 of 8 sentences]
22
[+] score: 25
Dysregulation of MIR101, MIR141, and MIR152 to the HIV-1 Gag protein contributes to HIV-1 budding and release via DNA hypermethylation, ubiquitin transfer, and endoplasmic reticulum -associated degradation at the late infection stage Briefly, dysregulation of; dysregulation of MIR9 contributes to HIV-1 infection to hijack CD4+ T cells through dysfunction of the immune and hormone pathways; dysregulation of MIR139-5p, MIRLET7i, and MIR10a contributes to the HIV-1 integration/replication stage through DNA hypermethylation and immune system dysfunction; dysregulation of MIR101, MIR141, and MIR152 contributes to the HIV-1 virus assembly/budding stage through DNA hypermethylation, ubiquitin transfer, and endoplasmic reticulum -associated degradation; dysregulation of MIR302a contributes to not only microvesicle -mediated transfer of miRNAs but also dysfunction of NF-κB signaling pathway in hepatocarcinogenesis. [score:7]
We found that dysregulation of; dysregulation of MIR9 contributes to HIV-1 infection to hijack CD4+ T cells through dysfunction of the immune and hormone pathways; dysregulation of MIR139-5p, MIRLET7i, and MIR10a contributes to the HIV-1 integration/replication stage; dysregulation of MIR101, MIR141, and MIR152 contributes to the HIV-1 virus assembly and budding mechanisms; dysregulation of MIR302a contributes to not only microvesicle -mediated transfer of miRNAs but also dysfunction of NF-κB signaling pathway in hepatocarcinogenesis. [score:6]
Therefore, the expression changes of MIR101, MIR141, and MIR152 (p-value < 0.037, p-value < 0.108, and p-value < 0.126, respectively) contributed to the expression change of Gag (p-value < 0.090). [score:5]
At the late infection stage, we determined that regulation of MIR101, MIR141, and MIR152 to Gag (p-value < 1☓10 [-16]) results in dysfunction of the infected cells through a signaling cascade of 5 proteins, PRMT1, inositol 1,4,5-trisphosphate receptor type 1 (ITPR1), autocrine motility factor receptor (AMFR), tripartite motif containing 25 (TRIM25), and ubiquitin-conjugating enzyme E2N (UBE2N) (Fig.   7). [score:2]
Therefore, we suggested that the UBE2N -associated ubiquitin transfer is induced by a signaling cascade leading to dysregulation of MIR101, MIR141, and MIR152. [score:2]
Dysregulation of MIR101, MIR141, and MIR152 to HIV-1 budding and releasing through DNA hypermethylation, ubiquitin transfer, and endoplasmic reticulum -associated degradation at the virus assembly/budding infection stage. [score:2]
It has been also suggested that MIR101 [110], and MIR152 [111] induce aberrant DNA hypermethylation in the hepatitis B virus infection. [score:1]
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23
[+] score: 23
Yao et al. reported that LncRNA XIST was highly expressed in glioma stem cells, and the results of this study showed that knockdown of the LncRNA XIST in glioma cells could lead to miR-152 upregulation, which resulted in the inhibition of CSCs [67]. [score:9]
Knockdown of the LncRNA XIST in glioma cells could lead to miR-152 upregulation, which resulted in the inhibition of CSCs (HCC) is a global health problem and is ranked sixth worldwide for malignant tumors [38]. [score:7]
Knockdown of the LncRNA XIST in glioma cells could lead to miR-152 upregulation, which resulted in the inhibition of CSCs Research regarding the effect and mechanism of LncRNAs on CSCs’ self-renewal and malignant transformation is still in the initial stages. [score:7]
[1 to 20 of 3 sentences]
24
[+] score: 22
Other miRNAs from this paper: hsa-mir-148a, hsa-mir-148b, hsa-mir-628, hsa-mir-548q
In addition, miR-152 overexpression repressed HLA-G upregulation induced by TGF- β. Finally, the authors observed that miR-152 expression levels were inversely correlated to both HLA-G and TGF- β levels in GC patients. [score:8]
Furthermore, TGF- β also inhibited miR-152 expression, and HLA-G was posttranscriptionally regulated by miR-152. [score:6]
Expression and function of HLA-G and regulatory microRNA (miR-152, -148A, -148B, and -133A) have been analyzed by Jasinski-Bergner and colleagues in renal cell carcinoma (RCC). [score:4]
They suggested a potential application of miR-152 as therapeutic target or potential biomarker for GC patients [35]. [score:3]
The interactions between HLA-G and miR-152 (and TGF- β) have been also analyzed by Guan and colleagues in gastric cancer (GC). [score:1]
[1 to 20 of 5 sentences]
25
[+] score: 21
In SKBR3, along with the over -expression of miR-29b, miR-455 was also up-regulated whereas miR-152 did not show any significant change. [score:6]
To understand the molecular mechanism of miR-29b deregulation, we analyzed the co -expression profiles of two important upstream suppressors (miR-152 and miR-455) [71]. [score:6]
Both of miR-29b suppressors, miR-152 and miR-455, were over-expressed in MDA-MB231 cell line. [score:5]
These data suggest a prominent inhibitory effect of miR-152 rather than miR-455 on the regulation of miR-29b emphasizing the controlling effect of miRNAs in certain types of cancer. [score:4]
[1 to 20 of 4 sentences]
26
[+] score: 20
Other miRNAs from this paper: hsa-mir-222
miR-152, a tumor suppressor microRNA targeting DNMT1, was significantly down-regulated in nickel sulfide-transformed 16HBE cells [67]. [score:8]
Moreover, while ectopic expression of miR-152 in nickel sulfide-transformed cells inhibited cell proliferation, expressing anti-miR-152 in normal 16HBE cells resulted in increased cell proliferation and colony formation [67]. [score:7]
These results clearly demonstrate that down-regulation of miR-152 contributes to nickel sulfide -induced cell transformation. [score:4]
As a result, DNMT1 levels increased, which lead to elevated DNA methylation levels and enriched MeCP2 at the promoter of miR-152. [score:1]
[1 to 20 of 4 sentences]
27
[+] score: 20
Other miRNAs from this paper: hsa-mir-148a, hsa-mir-148b
The presence of guanine at position +3142 may increase the affinity for miR-148a, miR-148b, and miR-152, which may downregulate the expression of HLA-G by RNA degradation or translation suppression [151, 152]. [score:10]
The binding of miR-148a and miR-152 downregulates the expression of HLA-G by RNA degradation or translation suppression. [score:10]
[1 to 20 of 2 sentences]
28
[+] score: 18
To confirm formaldehyde -induced miRNA expression changes, we performed RT-PCR using two miRNAs identified as the most increased in expression (miR-125b and miR-152) and the two miRNAs identified as the most decreased in expression (miR-145 and miR-142-3p) after 6 ppm formaldehyde exposure. [score:7]
Specifically, the two miRNAs most increased in expression (miR-125b and miR-152) and the two miRNAs most decreased in expression (miR-145 and miR-142-3p) in response to 6 ppm formaldehyde were validated using this alternative method. [score:5]
More specifically, miR-142-3p, miR-145, miR-152, miR-203, miR-26b, and miR-29a have all been shown to have altered expression levels in nasopharyngeal cancer tissue in comparison to noncancerous tissue (Chen et al. 2009; Li et al. 2011; Sengupta et al. 2008; Wong et al. 2012). [score:3]
Comparing the exposed versus unexposed samples confirmed that miR-125b and miR-152, were, indeed, significantly (p < 0.05) increased in expression upon exposure to 6 ppm formaldehyde (Figure 1). [score:3]
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29
[+] score: 16
Notably, HCV downregulates miR-152 [45], which directly targets the WNT1 3′-UTR, thereby relieving the suppression and inducing Wnt1 -mediated signaling that promotes in proliferation, G1-S transition, and colony formation in HepG2 cells. [score:9]
Ad-HCV core adenovirus infection can downregulate miR-152 and upregulate the Wnt/β-catenin effector Wnt1 in HepG2 cells. [score:7]
[1 to 20 of 2 sentences]
30
[+] score: 15
Other miRNAs from this paper: hsa-mir-21, hsa-mir-23a, hsa-mir-25, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-30a, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-192, hsa-mir-148a, hsa-mir-30c-2, hsa-mir-30d, hsa-mir-10a, hsa-mir-10b, hsa-mir-34a, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-187, hsa-mir-181a-1, hsa-mir-221, hsa-mir-30b, hsa-mir-122, hsa-mir-125b-1, hsa-mir-125b-2, hsa-mir-146a, hsa-mir-193a, hsa-mir-181b-2, hsa-mir-30c-1, hsa-mir-34b, hsa-mir-34c, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-148b, hsa-mir-193b, hsa-mir-181d, hsa-mir-92b, hsa-mir-454, ssa-mir-10a-1, ssa-mir-10a-2, ssa-mir-10b-1, ssa-mir-10b-2, ssa-mir-10b-3, ssa-mir-10b-4, ssa-mir-10d-1, ssa-mir-10d-2, ssa-mir-122-1, ssa-mir-122-2, ssa-mir-125b-1, ssa-mir-125b-2, ssa-mir-125b-3, ssa-mir-146a-1, ssa-mir-146a-2, ssa-mir-146a-3, ssa-mir-148a, ssa-mir-148b, ssa-mir-152, ssa-mir-16a-1, ssa-mir-16a-2, ssa-mir-181a-1, ssa-mir-181a-2, ssa-mir-181a-3, ssa-mir-181a-4, ssa-mir-181a-5, ssa-mir-181b, ssa-mir-181c, ssa-mir-192a-1, ssa-mir-192a-2, ssa-mir-192b, ssa-mir-193, ssa-mir-21a-1, ssa-mir-21a-2, ssa-mir-21b, ssa-mir-221, ssa-mir-23a-3, ssa-mir-23a-4, ssa-mir-23a-1, ssa-mir-23a-2, ssa-mir-25-1, ssa-mir-25-2, ssa-mir-25-3, ssa-mir-26a-1, ssa-mir-26a-2, ssa-mir-26a-3, ssa-mir-26a-4, ssa-mir-26a-5, ssa-mir-26a-6, ssa-mir-26b, ssa-mir-26d, ssa-mir-30a-3, ssa-mir-30a-4, ssa-mir-30a-1, ssa-mir-30a-2, ssa-mir-30b, ssa-mir-30c-1, ssa-mir-30c-2, ssa-mir-30d-1, ssa-mir-30d-2, ssa-mir-30e-1, ssa-mir-30e-2, ssa-mir-30e-3, ssa-mir-454, ssa-mir-462a, ssa-mir-92a-1, ssa-mir-92a-2, ssa-mir-92a-3, ssa-mir-92a-4, ssa-mir-92b
From day 2 of the exposure period to day 28, all but one of the examined miRNAs followed two distinct trends: one group of miRNAs was up-regulated (MiR10b-5p, MiR21a-3p, MiR23a-3p, MiR125b-1-3p, MiR221-3p), while the other group was down-regulated (MiR92b-3p, MiR122-5p, MiR122-2-3p, MiR152-5p). [score:7]
Several up-regulated (MiR21a-3p, MiR125b-1-3p, MiR23a-3p, MiR10b-5p, MiR221-3p) and down-regulated (MiR92b-3p, MiR152-5p, MiR122-2-3p or MiR122-5p) miRNAs shown in Fig 4A have been implicated in cirrhosis and hepatocellular carcinoma in humans [31]. [score:7]
At 1 d, there was significantly more of the miRNAs in the MC-LR group than in the control group, with the exception of MiR10b-5p, MiR122-2-3p, and MiR152-5p. [score:1]
[1 to 20 of 3 sentences]
31
[+] score: 14
The authors also revealed a correlation between the overexpression of H19 and DNMT1 and the downregulation of miR-152 in human breast tumor tissues. [score:6]
In human breast cancer cells lines, H19 upregulates the DNA methyltransferase DNMT1 by sponging miR-152, leading to enhancement of cell proliferation and invasion of the cells [61]. [score:4]
As described in Section 3.2, H19 impairs availability of miR-152 and increases the expression of the epigenetic regulator DNMT1 and so increases proliferation of breast cancer cells lines [61]. [score:4]
[1 to 20 of 3 sentences]
32
[+] score: 14
For example, among the 23 miRNAs with age-limited expression and 101 differentially expressed miRNAs, one (miR-652) was up-regulated in schizophrenia (Lai et al., 2011), and three others were either down-regulated (miR-152) or up-regulated (miR-133b and miR-7) in bronchopulmonary dysplasia (Wu et al., 2013), all in peripheral blood. [score:14]
[1 to 20 of 1 sentences]
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[+] score: 13
It was found that miR-152 was downregulated by HBx protein, causing an upregulation of its target DNA methyltransferase 1 expression and subsequently methylation of tumor suppressor genes to induce HCC 42. [score:13]
[1 to 20 of 1 sentences]
34
[+] score: 13
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-mir-21, hsa-mir-26a-1, hsa-mir-27a, hsa-mir-28, hsa-mir-30a, hsa-mir-96, hsa-mir-98, hsa-mir-99a, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-196a-1, hsa-mir-199a-1, hsa-mir-148a, hsa-mir-30d, hsa-mir-34a, hsa-mir-196a-2, hsa-mir-199a-2, hsa-mir-23b, hsa-mir-27b, hsa-mir-125b-1, hsa-mir-143, hsa-mir-145, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-194-1, hsa-mir-194-2, hsa-mir-200a, hsa-mir-99b, hsa-mir-26a-2, hsa-mir-378a, hsa-mir-342, hsa-mir-148b, hsa-mir-338, hsa-mir-335, hsa-mir-196b, hsa-mir-484, hsa-mir-486-1, hsa-mir-1271, hsa-mir-378d-2, bta-mir-26a-2, bta-mir-103-1, bta-mir-148a, bta-mir-21, bta-mir-27a, bta-mir-30d, bta-mir-484, bta-mir-99a, bta-mir-125a, bta-mir-125b-1, bta-mir-145, bta-mir-199a-1, bta-mir-27b, bta-mir-98, bta-mir-148b, bta-mir-200a, bta-mir-30a, bta-let-7a-1, bta-mir-342, bta-mir-23b, bta-let-7a-2, bta-let-7a-3, bta-mir-103-2, bta-mir-125b-2, bta-mir-34a, bta-mir-99b, hsa-mir-885, hsa-mir-103b-1, hsa-mir-103b-2, bta-mir-143, bta-mir-152, bta-mir-16a, bta-mir-194-2, bta-mir-196a-2, bta-mir-196a-1, bta-mir-196b, bta-mir-199a-2, bta-mir-26a-1, bta-mir-28, bta-mir-335, bta-mir-338, bta-mir-378-1, bta-mir-486, bta-mir-885, bta-mir-96, bta-mir-1271, bta-mir-2299, bta-mir-199c, bta-mir-1388, bta-mir-194-1, bta-mir-378-2, hsa-mir-378b, bta-mir-3431, hsa-mir-378c, hsa-mir-4286, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-378f, hsa-mir-378g, hsa-mir-378h, hsa-mir-378i, bta-mir-4286-1, bta-mir-4286-2, hsa-mir-378j, bta-mir-378b, bta-mir-378c, hsa-mir-486-2, bta-mir-378d, bta-mir-194b, bta-mir-194b-2
For those miRNAs (bta-miR-199c, miR-3431, miR-2299-5p, miR-152 and miR-1388-5p) without target information in IPA database, we used the perl scripts from the TargetScan website (http://targetscan. [score:7]
When compared with the control period (day-14), we identified a total of 22 DE miRNAs at day+28 including 10 up-regulated (bta-miR-199c, miR-199a-3p, miR-98, miR-378, miR-21-5p, miR-148b, miR-34a, miR-152, miR-16a, and miR-28) and 12 down-regulated (bta-miR-200a, miR-145, miR-99a-5p, miR-125b, miR-99b, miR-125a, miR-96, miR-484, miR-1388-5p, miR-342, miR-486 and miR-1271) (Table  2). [score:6]
[1 to 20 of 2 sentences]
35
[+] score: 13
For example, miR-100 and miR-199a-3p suppress mTOR expression [20- 22], and miR-152 and miR-218 suppress Rictor in some cancers [23, 24]. [score:7]
Two other miRNAs that also target Rictor, miR-218 and miR-152, has shown to be downregulated in oral squamous cell carcinoma and endometrial cancer [23, 24]. [score:6]
[1 to 20 of 2 sentences]
36
[+] score: 13
For instance, TUBG1 is inhibited by mir-152, STMN1 is inhibited by mir-210, LRRFIP2 and UNG are inhibited by mir-214, GCN1L1 is inhibited by mir-221, RPL37 is inhibited by mir-381, and PIGN is inhibited by mir-320a and mir-653. [score:13]
[1 to 20 of 1 sentences]
37
[+] score: 13
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-16-1, hsa-mir-17, hsa-mir-20a, hsa-mir-21, hsa-mir-28, hsa-mir-29a, hsa-mir-93, hsa-mir-100, hsa-mir-101-1, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-107, hsa-mir-16-2, hsa-mir-196a-1, hsa-mir-199a-1, hsa-mir-148a, hsa-mir-34a, hsa-mir-181c, hsa-mir-182, hsa-mir-196a-2, hsa-mir-199a-2, hsa-mir-210, hsa-mir-217, hsa-mir-223, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-15b, hsa-mir-27b, hsa-mir-122, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-125b-1, hsa-mir-130a, hsa-mir-132, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-137, hsa-mir-138-2, hsa-mir-141, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-134, hsa-mir-138-1, hsa-mir-146a, hsa-mir-150, hsa-mir-200c, hsa-mir-1-1, hsa-mir-155, hsa-mir-106b, hsa-mir-29c, hsa-mir-101-2, hsa-mir-34b, hsa-mir-34c, hsa-mir-372, hsa-mir-382, hsa-mir-148b, hsa-mir-196b, hsa-mir-424, hsa-mir-448, hsa-mir-449a, hsa-mir-483, hsa-mir-491, hsa-mir-501, hsa-mir-503, hsa-mir-548a-1, hsa-mir-548b, hsa-mir-548a-2, hsa-mir-548a-3, hsa-mir-548c, hsa-mir-548d-1, hsa-mir-548d-2, hsa-mir-320c-1, hsa-mir-548e, hsa-mir-548j, hsa-mir-548k, hsa-mir-548l, hsa-mir-548f-1, hsa-mir-548f-2, hsa-mir-548f-3, hsa-mir-548f-4, hsa-mir-548f-5, hsa-mir-548g, hsa-mir-548n, hsa-mir-548m, hsa-mir-548o, hsa-mir-548h-1, hsa-mir-548h-2, hsa-mir-548h-3, hsa-mir-548h-4, hsa-mir-548p, hsa-mir-548i-1, hsa-mir-548i-2, hsa-mir-548i-3, hsa-mir-548i-4, hsa-mir-320c-2, hsa-mir-548q, hsa-mir-548s, hsa-mir-548t, hsa-mir-548u, hsa-mir-548v, hsa-mir-548w, hsa-mir-548x, hsa-mir-548y, hsa-mir-548z, hsa-mir-548aa-1, hsa-mir-548aa-2, hsa-mir-548o-2, hsa-mir-548h-5, hsa-mir-548ab, hsa-mir-548ac, hsa-mir-548ad, hsa-mir-548ae-1, hsa-mir-548ae-2, hsa-mir-548ag-1, hsa-mir-548ag-2, hsa-mir-548ah, hsa-mir-548ai, hsa-mir-548aj-1, hsa-mir-548aj-2, hsa-mir-548x-2, hsa-mir-548ak, hsa-mir-548al, hsa-mir-548am, hsa-mir-548an, hsa-mir-548ao, hsa-mir-548ap, hsa-mir-548aq, hsa-mir-548ar, hsa-mir-548as, hsa-mir-548at, hsa-mir-548au, hsa-mir-548av, hsa-mir-548aw, hsa-mir-548ax, hsa-mir-548ay, hsa-mir-548az, hsa-mir-548ba, hsa-mir-548bb, hsa-mir-548bc
Similarly, up-regulation of miR-155 and miR-141, as well as down-regulation of miR-152 and miR-491 (which are tumor suppressors), promotes hepatocellular carcinoma in HCV infection [43, 65]. [score:9]
Whereas, miR-152 reduces the levels of DNA methyltransferase 1 (DNMT1) in HBV induced Hepatocellular carcinoma by targeting 3′UTR of DNMT1 [115]. [score:3]
Two of the miRNA namely miR-1 and miR-152 are reported to be involved in HBV pathogenesis via epigenetic control [114, 115]. [score:1]
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38
[+] score: 13
miR-152 expression has been found to be higher and conversely, HLA-G expression to be lower in PE. [score:5]
Thus, it is tempting to speculate that miR-152 may play a role in regulating HLA-G expression in PE. [score:4]
HLA-G is known to be involved in developing immune tolerance in pregnancy and miR-152 has been shown to repress HLA-G expression in JEG-3 choriocarcinoma cells. [score:3]
Furthermore, miR-152 plays a role as an immune response enhancer by increasing NK cell -mediated cytolysis (51). [score:1]
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39
[+] score: 12
There are also a number of miRNAs such as miR-132, miR-212, miR-130a and miR-152 shown to be upregulated in the pancreatic islets of the wi dely-studied T2D mo del Goto-Kakizaki rats (Esguerra et al., 2011) with active roles in beta cell stimulus-secretion coupling (Malm et al., 2016; Ofori et al., 2017). [score:4]
Expression of miR-200a, miR-130a and miR-152 in INS-1 832/13 cells (A–C) or in EndoC-βH1 cells (D–F) at different confluences. [score:3]
For miR-200a, miR-130a and miR-152, the expression levels were found not to be influenced by cellular confluence (Fig. S2). [score:3]
We also investigated the influence of confluence on the expression levels of miR-200a, miR-130a, miR-152, miR-132 and miR-212. [score:1]
The following primers from TaqMan [®] Gene Expression and TaqMan [®] miRNA Assays were used for qPCR: Cav1/CAV1 (Rn00755834_m1/Hs00971716_m1), Aifm1/AIFM1 (Rn00442540_m1/ Hs00377585_m1), miR-375 (TM_ 000564), miR-200a (TM_000502), miR-130a (TM_00454), miR-152 (TM_000475), miR-132 (TM_000457) and miR-212 (TM_002551) were used for qPCR. [score:1]
[1 to 20 of 5 sentences]
40
[+] score: 12
The downregulation of KLF4 by overexpressing miR-152 leads to attenuation of the activation of MEK1/2 and PI3K signal pathways [75]. [score:6]
In vivo as well as in vitro data explored the role of miR-152 as a tumor suppressor in GBM stem cells [75]. [score:3]
Krüppel-like factor 4 (KLF4) was suggested as the downstream target of miR-152. [score:3]
[1 to 20 of 3 sentences]
41
[+] score: 12
Knockdown of long non-coding RNA XIST exerts tumor-suppressive functions in human glioblastoma stem cells by up -regulating miR-152. [score:5]
Furthermore, the knockdown of the lncRNA XIST could exert tumor-suppressive effects in human GBM stem cells by up -regulating miR-152 (Yao et al., 2015). [score:5]
Furthermore, as XIST and miR-152 may form a reciprocal repression feedback loop and are located in the same RNA induced silencing complex (RISC), miR-152 can mediate the promotion of GSCs by XIST (Yao et al., 2015). [score:1]
In this regard, recent studies have demonstrated that lncRNAs in gliomas can serve as molecular decoys, which move proteins or RNAs away from a specific location, like a “sponge” to miRNAs (e. g., HOTAIR/miR-326, CASC2/miR-21, XIST/miR-152, and Gas5/miR-222). [score:1]
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42
[+] score: 11
The most representative ones were miR-212, miR-026a, miR-150, miR-152, miR-191, and miR-192, which were upregulated in pituitary adenomas, while miR-024-1 and miR-098 were downregulated in tumor samples. [score:7]
Study of Cheng et al. suggested that the upregulated miR-150, miR-152, miR-191, and miR-192 may also be involved in apoptosis [84]. [score:4]
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43
[+] score: 11
Methylation of miR-152 and miR-10b-5p promoted multiple myeloma (MM) progression by upregulating expression of specific oncogenes (DNMT1, BTRC, MYCBP and E2F3) [75]. [score:6]
Another study showed that miR-152 functions as a tumor suppressor in EC, and E2F3, MET, and Rictor were identified as novel candidate targets of miR-152 [37]. [score:5]
[1 to 20 of 2 sentences]
44
[+] score: 11
5) 7 hsa-mir-19a dbDEMC 32 hsa-mir-30d dbDEMC 8 hsa-mir-92a HMDD, miR2Disease 33 hsa-mir-451 literature 9 hsa-mir-210 miR2Disease 34 hsa-mir-152 dbDEMC 10 hsa-mir-19b dbDEMC, miR2Disease 35 hsa-mir-215 dbDEMC 11 hsa-mir-224 dbDEMC, miR2Disease 36 hsa-mir-130a dbDEMC, HMDD 12 hsa-let-7f dbDEMC, miR2Disease 37 hsa-mir-499 higher RWRMDA (No. [score:11]
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45
[+] score: 11
The expression of DNMT1 is thus inversely related to the expression miRNA-148a and its family homolog miRNA-152 [57, 58]. [score:5]
The forced expression of miRNA-152 in dairy cow MECs resulted in a marked reduction of DNMT1 at both the mRNA and protein levels [55]. [score:3]
Wang et al. [55] reported that the expression of miRNA-152 significantly increased during lactation in MECs of dairy cows producing high quality milk compared to lower miRNA-152 levels in cows producing low quality milk. [score:2]
miRNA-148a, miRNA-148b, and miRNA-152 are three members of the miRNA-148/152 family, which shares substantial homology in their seed sequences [54]. [score:1]
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[+] score: 11
We normalized the expression levels of the 162 microRNAs against miR-152 expression levels in all 12 samples for further analysis. [score:5]
We used miR-152 as an endogenous normalization control, since its expression was not altered during different stages of erythroid differentiation [14], and it showed the least amount of variation across 40 different human tissues in a separate microRNA real-time RT-PCR profiling study (Applied Biosystems, unpublished data). [score:3]
The resulting negative normalized Ct value (as represented by −ΔCt [i] = −(Ct [i]−Ct [miR152])) of all remaining 161 microRNAs indicated the expression level of each microRNA (detailed in supplemental website). [score:3]
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[+] score: 11
Figure S2 Expression levels of miR-27b, miR-151 and miR-152 in human circulating monocytes from postmenopausal women with low and high BMD as shown by qRT-PCR. [score:3]
In this study, we further selected four marginal differentially expressed miRNAs in the array study [23] for qRT-PCR validations, which are miR-27b, miR-422a, miR-151, and miR-152. [score:3]
Figure S1 Expression levels of miR-27b, miR-151 and miR-152 in human circulating monocytes from postmenopausal women with low and high BMD as shown by miRNA array. [score:3]
0.98±0.41, P = 0.30) and miR-152 (1.50±1.11 vs. [score:1]
0.86±0.42, P = 0.076), and miR-152 (1.32±0.49 vs. [score:1]
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[+] score: 11
Down-regulated microRNA-152 induces aberrant DNA methylation in hepatitis B virus-related hepatocellular carcinoma by targeting DNA methyltransferase 1. Hepatology 52 60– 70 10.1002/hep. [score:6]
For example, miR-152 acts as a tumor suppressor via suppression of DNMT1 (Huang et al., 2010). [score:5]
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49
[+] score: 11
Recently, Xiang et al. [32] reported that miR-152 and miR-185 were significantly downregulated in the S KOV3/DDP and A2780/DDP cells, compared with their sensitive parent line S KOV3 and A2780, and up -regulating the expression of miR-152 or miR-185 increased cisplatin sensitivity of S KOV3/DDP and A2780/DDP cells by suppressing DNA methyltransferase 1 (DNMT1) directly. [score:9]
Inconsistently, miR-152 and miR-185(decreased by 0.4 and 0.6 times in A2780/DDP cells compared with A2780 cells in Xiang’s study) was found to be up- or down-regulated in less than two times in A2780/DDP cells compared with A2780 cells, so these miRNAs were not listed as miRNAs of interest. [score:2]
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50
[+] score: 11
miRNA target has-miR302a MECP2 hsa-miR29a TET1, TET2, TET3 has-miR29a/c DNMT3A, DNMT3B has-miR29b-1/2 DNMT1 (Indirect via SP1) hsa-miR148a DNMT3B hsa-miR148a DNMT1 hsa-miR152 DNMT1 has-miR302a DNMT1 (Indirect via AOF2) hsa-miR342 DNMT1 hsa-miR17-92 DNMT1 hsa-miR26a-1/2 EZH2 hsa-miR101-1/2 EZH2/EED hsa-miR214 EZH2 hsa-miR128-1/2 BMI-1 hsa-miR199a-1/2 BRM hsa-miR433 HDAC6 hsa-miR449a HDAC1 hsa-miR138 SIRT1In the first column we report a list of miRNAs which are known to target epigenetic regulators and in the second column the corresponding targets. [score:10]
It is well known (see for instance Gruber and Zavolan, 2013) that Dnmt proteins are strictly controlled in a coordinated way by a number of miRNAs, among them in particular mir-29a/b/c, mir-152, mir148a, mir342, mir302 and various members of the cluster mir17-92. [score:1]
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51
[+] score: 10
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-16-1, hsa-mir-21, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-26a-1, hsa-mir-29a, hsa-mir-30a, hsa-mir-31, hsa-mir-99a, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-16-2, hsa-mir-192, hsa-mir-148a, hsa-mir-10b, hsa-mir-181a-2, hsa-mir-181a-1, hsa-mir-215, hsa-mir-223, hsa-mir-224, hsa-mir-200b, hsa-mir-15b, hsa-mir-27b, hsa-mir-125b-1, hsa-mir-141, hsa-mir-143, hsa-mir-125b-2, hsa-mir-126, hsa-mir-146a, hsa-mir-184, hsa-mir-200c, hsa-mir-155, hsa-mir-29c, hsa-mir-200a, hsa-mir-99b, hsa-mir-296, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-378a, hsa-mir-342, hsa-mir-148b, hsa-mir-451a, ssc-mir-125b-2, ssc-mir-148a, ssc-mir-15b, ssc-mir-184, ssc-mir-224, ssc-mir-23a, ssc-mir-24-1, ssc-mir-26a, ssc-mir-29b-1, ssc-let-7f-1, ssc-mir-103-1, ssc-mir-21, ssc-mir-29c, hsa-mir-486-1, hsa-mir-499a, hsa-mir-671, hsa-mir-378d-2, bta-mir-26a-2, bta-mir-29a, bta-let-7f-2, bta-mir-103-1, bta-mir-148a, bta-mir-16b, bta-mir-21, bta-mir-499, bta-mir-99a, bta-mir-125b-1, bta-mir-126, bta-mir-181a-2, bta-mir-27b, bta-mir-31, bta-mir-15b, bta-mir-215, bta-mir-30e, bta-mir-148b, bta-mir-192, bta-mir-200a, bta-mir-200c, bta-mir-23a, bta-mir-29b-2, bta-mir-29c, bta-mir-10b, bta-mir-24-2, bta-mir-30a, bta-mir-200b, bta-let-7a-1, bta-mir-342, bta-let-7f-1, bta-let-7a-2, bta-let-7a-3, bta-mir-103-2, bta-mir-125b-2, bta-mir-15a, bta-mir-99b, hsa-mir-664a, ssc-mir-99b, hsa-mir-103b-1, hsa-mir-103b-2, ssc-mir-15a, ssc-mir-16-2, ssc-mir-16-1, bta-mir-141, bta-mir-143, bta-mir-146a, bta-mir-152, bta-mir-155, bta-mir-16a, bta-mir-184, bta-mir-24-1, bta-mir-223, bta-mir-224, bta-mir-26a-1, bta-mir-296, bta-mir-29d, bta-mir-378-1, bta-mir-451, bta-mir-486, bta-mir-671, bta-mir-29e, bta-mir-29b-1, bta-mir-181a-1, ssc-mir-181a-1, ssc-mir-215, ssc-mir-30a, bta-mir-2318, bta-mir-2339, bta-mir-2430, bta-mir-664a, bta-mir-378-2, ssc-let-7a-1, ssc-mir-378-1, ssc-mir-29a, ssc-mir-30e, ssc-mir-499, ssc-mir-143, ssc-mir-10b, ssc-mir-486-1, ssc-mir-152, ssc-mir-103-2, ssc-mir-181a-2, ssc-mir-27b, ssc-mir-24-2, ssc-mir-99a, ssc-mir-148b, ssc-mir-664, ssc-mir-192, ssc-mir-342, ssc-mir-125b-1, oar-mir-21, oar-mir-29a, oar-mir-125b, oar-mir-181a-1, hsa-mir-378b, hsa-mir-378c, ssc-mir-296, ssc-mir-155, ssc-mir-146a, bta-mir-148c, ssc-mir-126, ssc-mir-378-2, ssc-mir-451, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-378f, hsa-mir-378g, hsa-mir-378h, hsa-mir-378i, hsa-mir-451b, hsa-mir-499b, ssc-let-7a-2, ssc-mir-486-2, hsa-mir-664b, hsa-mir-378j, ssc-let-7f-2, ssc-mir-29b-2, ssc-mir-31, ssc-mir-671, bta-mir-378b, bta-mir-378c, hsa-mir-486-2, oar-let-7a, oar-let-7f, oar-mir-103, oar-mir-10b, oar-mir-143, oar-mir-148a, oar-mir-152, oar-mir-16b, oar-mir-181a-2, oar-mir-200a, oar-mir-200b, oar-mir-200c, oar-mir-23a, oar-mir-26a, oar-mir-29b-1, oar-mir-30a, oar-mir-99a, bta-mir-664b, chi-let-7a, chi-let-7f, chi-mir-103, chi-mir-10b, chi-mir-125b, chi-mir-126, chi-mir-141, chi-mir-143, chi-mir-146a, chi-mir-148a, chi-mir-148b, chi-mir-155, chi-mir-15a, chi-mir-15b, chi-mir-16a, chi-mir-16b, chi-mir-184, chi-mir-192, chi-mir-200a, chi-mir-200b, chi-mir-200c, chi-mir-215, chi-mir-21, chi-mir-223, chi-mir-224, chi-mir-2318, chi-mir-23a, chi-mir-24, chi-mir-26a, chi-mir-27b, chi-mir-296, chi-mir-29a, chi-mir-29b, chi-mir-29c, chi-mir-30a, chi-mir-30e, chi-mir-342, chi-mir-378, chi-mir-451, chi-mir-499, chi-mir-671, chi-mir-99a, chi-mir-99b, bta-mir-378d, ssc-mir-378b, oar-mir-29b-2, ssc-mir-141, ssc-mir-200b, ssc-mir-223, bta-mir-148d
Ye et al. (2012) examined miRNA expression in the duodenum of E. coli F18-sensitive and -resistant weaned piglets and identified 12 candidate miRNA (ssc-miR-143, ssc-let-7f, ssc-miR-30e, ssc-miR-148a, ssc-miR-148b, ssc-miR-181a, ssc-miR-192, ssc-miR-27b, ssc-miR-15b, ssc-miR-21, ssc-miR-215, and ssc-miR-152) disease markers. [score:5]
In cattle, Wang et al. (2014) showed evidence that miRNA-152 regulates DNA methyltransferase 1 and is involved in the development and lactation processes in mammary glands. [score:3]
MicroRNA-152 regulates DNA methyltransferase 1 and is involved in the development and lactation of mammary glands in dairy cows. [score:2]
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[+] score: 10
miR-152 expression was dramatically downregulated in the cisplatin-resistant cell lines A2780/CP70 and S KOV3/DDP compared with their respective parental cells. [score:5]
Overexpression of miR-152 sensitized cisplatin-resistant ovarian cancer cells by reducing cisplatin -induced autophagy and enhancing cisplatin -induced apoptosis and inhibition of cell proliferation [85]. [score:5]
[1 to 20 of 2 sentences]
53
[+] score: 9
Irradiation with 10 Gy and PUFA treatment did not affect the expression of miR-34a, miR-96, miR-148a, miR-148b and miR-152 significantly (Additional file 1: Figure S1). [score:3]
with 10 Gy and PUFA treatment did not affect the expression of miR-34a, miR-96, miR-148a, miR-148b and miR-152 significantly (Additional file 1: Figure S1). [score:3]
with 10 Gy and PUFA treatment did not alter significantly the expression of miR-34a, miR-96, miR-148a, miR-148b and miR-152. [score:3]
[1 to 20 of 3 sentences]
54
[+] score: 9
Mir-152 targets HLA-G in JEG3 cells [42], miR-34a targets Notch1 and Jagged1 in HeLa and JAR cells [43], and miR-199b targets SET (protein phosphatase 2A inhibitor) in BeWo and JAR cells [44]. [score:9]
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55
[+] score: 9
MMP9 (a gelatinase that binds and degrades gelatin) is a direct target of miR-491-5p and miR-211-5p, which are both upregulated in tumor samples [35, 78, 79], and MMP3 (an archetypal metalloproteinase with stromelysin activity) is targeted by miR-152-3p [80]. [score:9]
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56
[+] score: 9
Among 20 expressed miRNAs, the expression levels of hsa-mir-25, hsa-mir-221, hsa-mir-302b, hsa-mir-363, hsa-mir-372, hsa-mir-199a, hsa-mir-302d, hsa-mir-26a, hsa-mir-320, hsa-mir-744, hsa-mir-152 and hsa-let-7e in the study of Morin et al. exceed those obtained with miRExpress, but the levels of hsa-mir-423, hsa-let-7a, hsa-mir-1, hsa-mir-340, hsa-mir-302a, hsa-mir-130a, hsa-let-7f and hsa-mir-122 in the work by Morin et al. are lower than those obtained from miRExpress (Table 6) (full data are available in additional file 7). [score:9]
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57
[+] score: 9
Moreover, ATP6AP2 interacting with microRNA-152 (a potential regulator of ATP6AP2) regulates downstream VEGF expression [12]. [score:5]
Moreover, ATP6AP2 interacting with microRNA-152 regulates downstream VEGF expression in hRECs [12]. [score:4]
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58
[+] score: 9
Other miRNAs from this paper: hsa-mir-186
For example, knockdown lncRNA XIST exerts tumor suppressive functions by up -regulating miR-152 in human glioblastoma stem cells [32]. [score:5]
In the case of glioma, lncRNA XIST exerts tumor-suppressive functions by up -regulating miR-152 in glioblastama stem cells [15]. [score:4]
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59
[+] score: 8
In another study, the activation of HSCs was inhibited by treatment with salvianolic acid B and the induced expression of miR-152 (Yu et al., 2015). [score:5]
Salvianolic acid b-Induced microRNA-152 inhibits liver fibrosis by attenuating DNMT1 -mediated patched1 methylation. [score:3]
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60
[+] score: 8
As for the potential regulatory miRNAs, only miR9748 and val-miR152 were predicted to target Curculin-like (mannose -binding) lectin family protein and viscotoxin, respectively. [score:4]
Contig1, which is highly homologous to Viscotoxin-A3 (90.99%), was predicted to be target of val-miR152. [score:3]
Contig1 90.99% 2.01E-53 val-miR152 Viscotoxin-B P08943.2 CL10031. [score:1]
[1 to 20 of 3 sentences]
61
[+] score: 8
Decreased XIST expression inhibited proliferation, migration and invasion, and promoted apoptosis of GSCs through binding and up-regulation of miR-152 [56]. [score:8]
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62
[+] score: 8
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-16-1, hsa-mir-17, hsa-mir-18a, hsa-mir-20a, hsa-mir-21, hsa-mir-29a, hsa-mir-33a, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-107, hsa-mir-16-2, mmu-let-7g, mmu-let-7i, mmu-mir-1a-1, mmu-mir-29b-1, mmu-mir-124-3, mmu-mir-126a, mmu-mir-9-2, mmu-mir-132, mmu-mir-133a-1, mmu-mir-134, mmu-mir-138-2, mmu-mir-145a, mmu-mir-152, mmu-mir-10b, mmu-mir-181a-2, hsa-mir-192, mmu-mir-204, mmu-mir-206, hsa-mir-148a, mmu-mir-143, hsa-mir-7-1, hsa-mir-7-2, hsa-mir-7-3, hsa-mir-10b, hsa-mir-34a, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-204, hsa-mir-211, hsa-mir-212, hsa-mir-181a-1, mmu-mir-34c, mmu-mir-34b, mmu-let-7d, mmu-mir-106b, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-132, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-138-2, hsa-mir-143, hsa-mir-145, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-126, hsa-mir-134, hsa-mir-138-1, hsa-mir-206, mmu-mir-148a, mmu-mir-192, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-15a, mmu-mir-16-1, mmu-mir-16-2, mmu-mir-18a, mmu-mir-20a, mmu-mir-21a, mmu-mir-29a, mmu-mir-29c, mmu-mir-34a, mmu-mir-330, hsa-mir-1-1, mmu-mir-1a-2, hsa-mir-181b-2, mmu-mir-107, mmu-mir-17, mmu-mir-212, mmu-mir-181a-1, mmu-mir-33, mmu-mir-211, mmu-mir-29b-2, mmu-mir-124-1, mmu-mir-124-2, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-138-1, mmu-mir-181b-1, mmu-mir-7a-1, mmu-mir-7a-2, mmu-mir-7b, hsa-mir-106b, hsa-mir-29c, hsa-mir-34b, hsa-mir-34c, hsa-mir-330, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, mmu-mir-181b-2, hsa-mir-181d, hsa-mir-505, hsa-mir-590, hsa-mir-33b, hsa-mir-454, mmu-mir-505, mmu-mir-181d, mmu-mir-590, mmu-mir-1b, mmu-mir-145b, mmu-mir-21b, mmu-let-7j, mmu-mir-21c, mmu-let-7k, mmu-mir-126b, mmu-mir-9b-2, mmu-mir-124b, mmu-mir-9b-1, mmu-mir-9b-3
MiR-152 inhibits proliferation of ovarian cancer cell lines and is regulated in axon guidance (Liu et al., 2012; Zhou et al., 2012). [score:3]
Altered expression of miR-152 and miR-148a in ovarian cancer is related to cell proliferation. [score:3]
A comparison of all 89 formaldehyde-modulated miRNAs in human lung epithelial cells (Rager et al., 2011) with the miRNAs predicted here to regulate genes in the brains of MAM -treated Mgmt [−/−] mice show overlap of 6 miRNAs: miR-107, miR-152, miR-17-5p, miR-181d, and miR-454-3p. [score:2]
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[+] score: 8
Zhu et al. reported that miR-152 could potentially controls migration and invasion by targeting TGF-α in prostate cancer cell lines [29]; Jin et al. reported that miR-376c could inhibit cell proliferation and invasion by targeting TGF-α in osteosarcoma [30]; Qin et al. reported that miR-124 may regulates TGF-α -induced EMT in human prostate cancer cells [31]. [score:8]
[1 to 20 of 1 sentences]
64
[+] score: 8
Additionally, activation of repair -mediated DNA demethylation (Barreto et al. 2007) and decreased expression and/or functioning of Dnmt1 caused by a number of factors, including direct effects of BD and its metabolites on Dnmt1 protein, aberrant expression of microRNAs (e. g., miR-29b, miR-148, and miR-152), and expression of chromatin-modifying proteins (Garzon et al. 2009; Huang et al. 2010; Vire et al. 2006; Wang et al. 2009), may further contribute to the loss of DNA methylation. [score:8]
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[+] score: 8
Here, we focus on four miRNAs, miR-152, -181c, -224 and -340, because we have already reported that miR-181c is epigenetically down-regulated in GC [13] and CpG islands are located in the upstream regions of three other miRNAs (Figure 2A and C, and Figure S1). [score:4]
As for miR-152 methylation analysis, we tried three primer sets designed in the upstream region of miR-152 containing CpG islands (Figure S1), but none of them completely matched miR-152 expression on MSP analyses (data not shown). [score:2]
Figure S1 Schematic representation of the COPZ2 region containing miR-152. [score:1]
A vertical arrow indicates the location of miR-152. [score:1]
[1 to 20 of 4 sentences]
66
[+] score: 7
Yao et al. discovered that knockdown of lncRNA XIST could exert tumor-suppressive functions in human glioblastoma stem cells by upregulating miR-152 [8]. [score:7]
[1 to 20 of 1 sentences]
67
[+] score: 7
The potential tumor suppressors miR-148a and miR-152 are important for breast cancer cell proliferation, colony formation, and angiogenesis by targeting IGF-IR and IRS1 and inhibiting their downstream PI3K/AKT and MAPK/ERK signaling pathways [13]. [score:7]
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68
[+] score: 7
The novel-miR-82, novel-miR-98, novel-miR-89 and novel-miR-84 miRNAs were downregulated, whilst the novel-miR-152 and novel-miR-15 miRNAs were upregulated (Table IV). [score:7]
[1 to 20 of 1 sentences]
69
[+] score: 7
Other miRNAs from this paper: hsa-mir-148a, hsa-mir-148b
The presence of a Guanine at the + 3142 is associated with a stronger binding of specific microRNAs, such as miR-148a, miR-148b, and miR-152, decreasing HLA-G expression by mRNA degradation and translation suppression (3, 158, 159). [score:7]
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70
[+] score: 7
Those miRNAs, we call them the epi-miRNAs, includes, for example, miR-148a, miR152, miR222 that targets mRNA of DNMTs and leads to re -expression of hyper-methylated tumor suppressors [32]. [score:7]
[1 to 20 of 1 sentences]
71
[+] score: 7
Other miRNAs from this paper: hsa-mir-148a, hsa-mir-184, hsa-mir-148b, hsa-mir-675
Wu et al. previously confirmed that miR-152 suppressed proliferation and migration of human umbilical vein endothelial cells (HUVECs) by targeting ADAM17 [29]. [score:5]
Yang et al. demonstrated that miR-148a and miR-152 were associated with homocysteine-facilitated foam cell differentiation and atherosclerotic lesion [30]. [score:1]
miR-148b is a member of miR-148/miR-152 family, which also contains miR-148a and miR-152 [28]. [score:1]
[1 to 20 of 3 sentences]
72
[+] score: 7
miRNA microarray studies have reported four upregulated miRNAs (miR-152, -410, -431, and -493) and four downregulated miRNAs (miR-15a, -20a, -25, and -155) in both replicative and stress -induced senescence [28]. [score:7]
[1 to 20 of 1 sentences]
73
[+] score: 7
Other miRNAs from this paper: hsa-let-7c, hsa-let-7d, hsa-mir-16-1, hsa-mir-21, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-28, hsa-mir-29a, hsa-mir-30a, hsa-mir-31, hsa-mir-99a, hsa-mir-101-1, hsa-mir-16-2, mmu-let-7g, mmu-let-7i, mmu-mir-27b, mmu-mir-30a, mmu-mir-99a, mmu-mir-101a, mmu-mir-125b-2, mmu-mir-126a, mmu-mir-128-1, mmu-mir-9-2, mmu-mir-142a, mmu-mir-144, mmu-mir-145a, mmu-mir-151, mmu-mir-152, mmu-mir-185, mmu-mir-186, mmu-mir-24-1, mmu-mir-203, mmu-mir-205, hsa-mir-148a, hsa-mir-34a, hsa-mir-203a, hsa-mir-205, hsa-mir-210, hsa-mir-221, mmu-mir-301a, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-27b, hsa-mir-125b-1, hsa-mir-128-1, hsa-mir-142, hsa-mir-144, hsa-mir-145, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125b-2, hsa-mir-126, hsa-mir-185, hsa-mir-186, mmu-mir-148a, mmu-mir-200a, mmu-let-7c-1, mmu-let-7c-2, mmu-mir-16-1, mmu-mir-16-2, mmu-mir-21a, mmu-mir-24-2, mmu-mir-29a, mmu-mir-31, mmu-mir-34a, mmu-mir-148b, mmu-mir-339, mmu-mir-101b, mmu-mir-28a, mmu-mir-210, mmu-mir-221, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-125b-1, mmu-mir-128-2, hsa-mir-128-2, hsa-mir-200a, hsa-mir-101-2, hsa-mir-301a, hsa-mir-151a, hsa-mir-148b, hsa-mir-339, hsa-mir-335, mmu-mir-335, hsa-mir-449a, mmu-mir-449a, hsa-mir-450a-1, mmu-mir-450a-1, hsa-mir-486-1, hsa-mir-146b, hsa-mir-450a-2, hsa-mir-503, mmu-mir-486a, mmu-mir-542, mmu-mir-450a-2, mmu-mir-503, hsa-mir-542, hsa-mir-151b, mmu-mir-301b, mmu-mir-146b, mmu-mir-708, hsa-mir-708, hsa-mir-301b, hsa-mir-1246, hsa-mir-1277, hsa-mir-1307, hsa-mir-2115, mmu-mir-486b, mmu-mir-28c, mmu-mir-101c, mmu-mir-28b, hsa-mir-203b, hsa-mir-5680, hsa-mir-5681a, mmu-mir-145b, mmu-mir-21b, mmu-mir-21c, hsa-mir-486-2, mmu-mir-126b, mmu-mir-142b, mmu-mir-9b-2, mmu-mir-9b-1, mmu-mir-9b-3
In a number of single studies, miRNAs such as let-7d [26], let-7i [26] and miR-210 [23] were also found to be up-regulated in prostate cancer, in contrast to let-7g [23], miR-27b [28], miR-99a [23], miR-126 [54], miR-128 [26], miR-152 [28], miR-200a [58] and miR-449a [59] which were down-regulated in prostate cancer samples. [score:7]
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74
[+] score: 7
For instance, mirPRo reported that mmu-miR-152-3p is down-regulated significantly (see mouse data alignments in) whereas miRDeep2 called it a miRNA without significant differential expression. [score:6]
mmu-miR-152-3p exemplifies the case (Δ/−) while has-miR-324-5p exemplifies the case (Δ/+) shown in Fig. 2. The alignment results from miRDeep2 are presented in Supplementary Data 12– 21. [score:1]
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75
[+] score: 6
miR-29a (Benetti et al., 2008), miR-152 (Fabbri et al., 2007), and the miR-17∼29 cluster (Dakhlallah et al., 2013) have all been shown to target DNA methyltransferase (DNMT), a key regulator of DNA methylation, thereby contributing to hepatocellular carcinoma, pulmonary fibrosis, and 16HBE cells. [score:4]
Various epi-miRNAs, including miR-29, miR-152, and miR-290, have been shown to play pivotal roles in regulating the epigenetic modifications that occur through DNA methylation (Ji et al., 2013). [score:2]
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76
[+] score: 6
Of note, in both uninfected and Mtb-infected macrophages, Sp110 induced miR-155, miR-342, miR-3470a and miR-532, but inhibited let-7e, miR-1249, miR-125a, miR-132, miR-152, miR-16-1, miR-182, miR-183, miR-23a, miR-28a, miR-5114, miR-99a and miR-99b. [score:3]
Moreover, Sp110 significantly inhibited the miR-99b-let-7e-125a cluster, miR-152, miR-21a, miR-23a and miR-27b (Fig. 5b,). [score:3]
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77
[+] score: 6
The top 4 positively correlated miRNAs, ranked by FDR (miR-193a-3p, miR-152, miR-31-5p and miR-34a-5p), have been described as tumor suppressor miRNAs 16– 19. [score:3]
The herein presented exposure signature of 93 miRNAs showed an overlap of 28 (30%) miRNAs with the diagnostic lymphoma signature (including the tumor suppressor miRNAs mir-193, miR-152 and miR-34a). [score:3]
[1 to 20 of 2 sentences]
78
[+] score: 6
It is reported that expression levels of some miR genes (including intragenic miR-152 and miR-34a/b/c and extragenic miR-203, miR-124-1/124-2, miR-129-2, and miR-181c) inversely correlate with methylation of their corresponding CpG islands [11, 13, 14, 16, 27, 38, 44]. [score:3]
It has been suggested that methylation of the CpG islands that are associated with miR genes (i. e. miR-203, miR-152, miR-124-1, miR-34b/c, miR-129-2, miR-9-1, miR-130b, miR-124-2, and miR-181c) might inversely correlate with their expression levels [12- 17]. [score:3]
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79
[+] score: 6
In our results, we did not find any correlation between miR-29c expression and the level of IFN- γ. Furthermore, upregulation of the miR-148 family (miR-148a, miR-148b, and miR-152) was observed in DCs stimulated by LPS. [score:6]
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80
[+] score: 6
This finding was consistent with a previous report that XIST functions as tumor suppressor by upregulating miR-152 in a RISC -dependent manner, and harbors a miR-152 binding site that allows XIST function as a ceRNA of miR-152 in GBM stem cells [32]. [score:6]
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81
[+] score: 5
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-16-1, hsa-mir-17, hsa-mir-20a, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-29a, hsa-mir-30a, hsa-mir-93, hsa-mir-101-1, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-107, hsa-mir-16-2, mmu-let-7g, mmu-let-7i, mmu-mir-15b, mmu-mir-23b, mmu-mir-29b-1, mmu-mir-30a, mmu-mir-30b, mmu-mir-101a, mmu-mir-124-3, mmu-mir-125a, mmu-mir-130a, mmu-mir-9-2, mmu-mir-135a-1, mmu-mir-136, mmu-mir-138-2, mmu-mir-140, mmu-mir-144, mmu-mir-145a, mmu-mir-146a, mmu-mir-149, mmu-mir-152, mmu-mir-10b, mmu-mir-181a-2, mmu-mir-182, mmu-mir-183, mmu-mir-185, mmu-mir-24-1, mmu-mir-191, mmu-mir-193a, mmu-mir-195a, mmu-mir-200b, mmu-mir-204, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-30e, hsa-mir-7-1, hsa-mir-7-2, hsa-mir-7-3, hsa-mir-10a, hsa-mir-10b, hsa-mir-34a, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-182, hsa-mir-183, hsa-mir-204, hsa-mir-181a-1, hsa-mir-221, hsa-mir-222, hsa-mir-200b, mmu-mir-301a, mmu-mir-34c, mmu-mir-34b, mmu-let-7d, mmu-mir-130b, hsa-let-7g, hsa-let-7i, hsa-mir-15b, hsa-mir-23b, hsa-mir-30b, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-130a, hsa-mir-135a-1, hsa-mir-135a-2, hsa-mir-138-2, hsa-mir-140, hsa-mir-144, hsa-mir-145, hsa-mir-191, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125a, hsa-mir-136, hsa-mir-138-1, hsa-mir-146a, hsa-mir-149, hsa-mir-185, hsa-mir-193a, hsa-mir-195, hsa-mir-320a, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-30d, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-15a, mmu-mir-16-1, mmu-mir-16-2, mmu-mir-20a, mmu-mir-23a, mmu-mir-24-2, mmu-mir-26a-1, mmu-mir-26b, mmu-mir-29a, mmu-mir-29c, mmu-mir-93, mmu-mir-34a, mmu-mir-330, mmu-mir-339, mmu-mir-340, mmu-mir-135b, mmu-mir-101b, hsa-mir-200c, hsa-mir-181b-2, mmu-mir-107, mmu-mir-10a, mmu-mir-17, mmu-mir-200c, mmu-mir-181a-1, mmu-mir-320, mmu-mir-26a-2, mmu-mir-221, mmu-mir-222, mmu-mir-29b-2, mmu-mir-135a-2, mmu-mir-124-1, mmu-mir-124-2, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-138-1, mmu-mir-181b-1, mmu-mir-181c, mmu-mir-7a-1, mmu-mir-7a-2, mmu-mir-7b, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-101-2, hsa-mir-34b, hsa-mir-34c, hsa-mir-301a, hsa-mir-130b, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-361, mmu-mir-361, hsa-mir-376a-1, mmu-mir-376a, hsa-mir-340, hsa-mir-330, hsa-mir-135b, hsa-mir-339, hsa-mir-335, mmu-mir-335, mmu-mir-181b-2, mmu-mir-376b, mmu-mir-434, mmu-mir-467a-1, hsa-mir-376b, hsa-mir-485, hsa-mir-146b, hsa-mir-193b, hsa-mir-181d, mmu-mir-485, mmu-mir-541, hsa-mir-376a-2, hsa-mir-320b-1, hsa-mir-320c-1, hsa-mir-320b-2, mmu-mir-301b, mmu-mir-674, mmu-mir-146b, mmu-mir-467b, mmu-mir-669c, mmu-mir-708, mmu-mir-676, mmu-mir-181d, mmu-mir-193b, mmu-mir-467c, mmu-mir-467d, hsa-mir-541, hsa-mir-708, hsa-mir-301b, mmu-mir-467e, mmu-mir-467f, mmu-mir-467g, mmu-mir-467h, hsa-mir-320d-1, hsa-mir-320c-2, hsa-mir-320d-2, mmu-mir-467a-2, mmu-mir-467a-3, mmu-mir-467a-4, mmu-mir-467a-5, mmu-mir-467a-6, mmu-mir-467a-7, mmu-mir-467a-8, mmu-mir-467a-9, mmu-mir-467a-10, hsa-mir-320e, hsa-mir-676, mmu-mir-101c, mmu-mir-195b, mmu-mir-145b, mmu-let-7j, mmu-mir-130c, mmu-mir-30f, mmu-let-7k, mmu-mir-9b-2, mmu-mir-124b, mmu-mir-9b-1, mmu-mir-9b-3
The miRNA families that change expression in both mouse and human were: let-7, miR-7, miR-15, miR-101, miR-140, miR-152 (all validated by qPCR, P < 0.05), as well as miR-17, miR-34, miR-135, miR-144, miR-146, miR-301, miR-339, miR-368 (qPCR not performed). [score:3]
39E-0218mmu-miR-138-5pmir-1380.2612.849.05E-053.20E-0340mmu-miR-140-3pmir-1400.197.891.23E-031.94E-0246mmu-miR-144-3pmir-1440.256.882.38E-033.30E-0268mmu-miR-145-5pmir-1450.177.038.25E-037.73E-0248mmu-miR-146b-5pmir-1460.167.502.60E-033.38E-0225mmu-miR-152-3pmir-1480.196.472.22E-045.65E-0331mmu-miR-149-5pmir-1490.227.694.26E-048.75E-0314mmu-miR-16-5pmir-150.2910.942.74E-051. [score:1]
Additional confirmation for WGCNA-suggested interactions was obtained from TarBase, the database for validated interactions, where we found validated interactions between miRNAs and mRNAs that were positively correlated in our study but negatively correlated in previous publications: mmu-miR-34a-5p --| ACTB, mmu-miR-200b-3p --| ZEB2, mmu-miR-30a-5p --| TNRC6A, mmu-miR-152-3p --| CAMK2A, mmu-miR-200c-3p --| FLT1, mmu-miR-20a-5p --| ZBTB7A. [score:1]
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82
[+] score: 5
Up-regulated miRNAs in NSCLC included miR-142-5p, miR-148b, miR-148a, miR-369-3p, miR-215, miR-152 and miR-155, whereas down-regulated miRNAs were miR-373 and miR-138-I. Some of these miRNAs have a well-characterized association with cancer progression, e. g., miR-10b, miR-21, miR-30a, miR-30e, miR-125b, miR-141, miR-200b, miR-200c, and miR-205 [90]. [score:5]
[1 to 20 of 1 sentences]
83
[+] score: 5
An inverse correlation between expression of ZIC3 and miR-137, miR-152, miR-154 and miR-155; LIN28 and let-7c, miR-137 and miR-152 and NANOG and miR-199a and miR-199b expression was found in ASC and NTERA-2 cells (Figure 5). [score:5]
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84
[+] score: 5
Many potential targets of this particular miRNA clustered in extra cellular matrix (ECM) receptor interaction; miR-29a showed e. g. a calculated significant interaction with COL4A1 (mfe: −24.1 kcal/mol; P<0.002), while this target was also predicted to be co -targeted by miR-152 (mfe: −22.8 kcal/mol; P<0.01). [score:5]
[1 to 20 of 1 sentences]
85
[+] score: 5
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-17, hsa-mir-18a, hsa-mir-19a, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-20a, hsa-mir-22, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, hsa-mir-27a, hsa-mir-29a, hsa-mir-30a, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-98, hsa-mir-99a, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-106a, hsa-mir-148a, hsa-mir-30c-2, hsa-mir-30d, hsa-mir-10a, hsa-mir-10b, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-182, hsa-mir-181a-1, hsa-mir-221, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-15b, hsa-mir-27b, hsa-mir-30b, hsa-mir-130a, hsa-mir-191, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-185, hsa-mir-193a, hsa-mir-320a, hsa-mir-200c, hsa-mir-1-1, hsa-mir-181b-2, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-99b, hsa-mir-130b, hsa-mir-30e, hsa-mir-363, hsa-mir-374a, hsa-mir-375, hsa-mir-378a, hsa-mir-148b, hsa-mir-331, hsa-mir-339, hsa-mir-423, hsa-mir-20b, hsa-mir-491, hsa-mir-193b, hsa-mir-181d, hsa-mir-92b, hsa-mir-320b-1, hsa-mir-320c-1, hsa-mir-320b-2, hsa-mir-378d-2, bta-mir-29a, bta-let-7f-2, bta-mir-148a, bta-mir-18a, bta-mir-20a, bta-mir-221, bta-mir-27a, bta-mir-30d, bta-mir-320a-2, bta-mir-99a, bta-mir-181a-2, bta-mir-27b, bta-mir-30b, bta-mir-106a, bta-mir-10a, bta-mir-15b, bta-mir-181b-2, bta-mir-193a, bta-mir-20b, bta-mir-30e, bta-mir-92a-2, bta-mir-98, bta-let-7d, bta-mir-148b, bta-mir-17, bta-mir-181c, bta-mir-191, bta-mir-200c, bta-mir-22, bta-mir-29b-2, bta-mir-29c, bta-mir-423, bta-let-7g, bta-mir-10b, bta-mir-24-2, bta-mir-30a, bta-let-7a-1, bta-let-7f-1, bta-mir-30c, bta-let-7i, bta-mir-25, bta-mir-363, bta-let-7a-2, bta-let-7a-3, bta-let-7b, bta-let-7c, bta-let-7e, bta-mir-15a, bta-mir-19a, bta-mir-19b, bta-mir-331, bta-mir-374a, bta-mir-99b, hsa-mir-374b, hsa-mir-320d-1, hsa-mir-320c-2, hsa-mir-320d-2, bta-mir-1-2, bta-mir-1-1, bta-mir-130a, bta-mir-130b, bta-mir-152, bta-mir-181d, bta-mir-182, bta-mir-185, bta-mir-24-1, bta-mir-193b, bta-mir-29d, bta-mir-30f, bta-mir-339a, bta-mir-374b, bta-mir-375, bta-mir-378-1, bta-mir-491, bta-mir-92a-1, bta-mir-92b, bta-mir-9-1, bta-mir-9-2, bta-mir-29e, bta-mir-29b-1, bta-mir-181a-1, bta-mir-181b-1, bta-mir-320b, bta-mir-339b, bta-mir-19b-2, bta-mir-320a-1, bta-mir-193a-2, bta-mir-378-2, hsa-mir-378b, hsa-mir-320e, hsa-mir-378c, bta-mir-148c, hsa-mir-374c, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-378f, hsa-mir-378g, hsa-mir-378h, hsa-mir-378i, hsa-mir-378j, bta-mir-378b, bta-mir-378c, bta-mir-378d, bta-mir-374c, bta-mir-148d
In this study, three members of this family (miR-148a, miR-148b and miR-152, Figure 12H) showed modest expression levels, suggesting that miR-148 may be a stably expressed miRNA in exosomes of most mammals including pigs. [score:5]
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86
[+] score: 5
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-21, hsa-mir-22, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, hsa-mir-26b, hsa-mir-27a, hsa-mir-31, hsa-mir-33a, hsa-mir-99a, hsa-mir-100, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-199a-1, hsa-mir-148a, hsa-mir-147a, hsa-mir-34a, hsa-mir-182, hsa-mir-199a-2, hsa-mir-212, hsa-mir-221, hsa-mir-224, hsa-let-7g, hsa-let-7i, hsa-mir-27b, hsa-mir-30b, hsa-mir-125b-1, hsa-mir-130a, hsa-mir-132, hsa-mir-142, hsa-mir-145, hsa-mir-153-1, hsa-mir-153-2, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-127, hsa-mir-134, hsa-mir-200c, hsa-mir-106b, hsa-mir-361, hsa-mir-148b, hsa-mir-20b, hsa-mir-410, hsa-mir-202, hsa-mir-503, hsa-mir-33b, hsa-mir-643, hsa-mir-659, bta-let-7f-2, bta-mir-103-1, bta-mir-148a, bta-mir-21, bta-mir-221, bta-mir-26b, bta-mir-27a, bta-mir-99a, bta-mir-125a, bta-mir-125b-1, bta-mir-145, bta-mir-199a-1, bta-mir-27b, bta-mir-30b, bta-mir-31, bta-mir-127, bta-mir-142, bta-mir-20b, bta-let-7d, bta-mir-132, bta-mir-148b, bta-mir-200c, bta-mir-22, bta-mir-23a, bta-mir-29b-2, bta-mir-361, bta-let-7g, bta-mir-24-2, bta-let-7a-1, bta-let-7f-1, bta-let-7i, bta-mir-25, bta-let-7a-2, bta-let-7a-3, bta-let-7b, bta-let-7c, bta-let-7e, bta-mir-103-2, bta-mir-125b-2, bta-mir-34a, hsa-mir-708, hsa-mir-147b, hsa-mir-877, hsa-mir-940, hsa-mir-548j, hsa-mir-302e, hsa-mir-103b-1, hsa-mir-103b-2, bta-mir-100, bta-mir-106b, bta-mir-130a, bta-mir-134, bta-mir-147, bta-mir-152, bta-mir-153-1, bta-mir-153-2, bta-mir-182, bta-mir-24-1, bta-mir-199a-2, bta-mir-202, bta-mir-212, bta-mir-224, bta-mir-33a, bta-mir-33b, bta-mir-410, bta-mir-708, bta-mir-877, bta-mir-940, bta-mir-29b-1, bta-mir-148c, bta-mir-503, bta-mir-148d
This study demonstrated that eight miRNAs (miR-503, miR-21, miR-29b, miR-142-3p, miR-34a, miR-152, miR-25 and miR-130a) were highly expressed, while nine miRNAs (miR-125a, miR-199a-3p, miR-125b, miR-99a, let-7c, miR-145, miR-31, miR-202 and miR-27b) were expressed at lower level between the follicular and luteal stages in ovine ovarian tissues. [score:5]
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87
[+] score: 5
Other miRNAs from this paper: hsa-mir-126, hsa-mir-185, hsa-mir-200c, hsa-mir-377
Additionally, post-transcriptional gene silencing by microRNAs, including miR-152, miR-185, miR-126 and miR-377, which directly interact with the3'-UTR of DMNT1 mRNA, could be important in the regulation of DMNT1 expression [14- 17]. [score:5]
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88
[+] score: 5
Other miRNAs from this paper: hsa-mir-193a, hsa-mir-376c
In the meta-analysis, we demonstrated that high expression of linc00152 was positively correlated with advanced LNM (OR = 2.49, 95% CI: 1.57–3.94); nevertheless abnormal miR-152 expression exerted no statistical significance in VI (OR = 1.02, 95% CI: 0.54–1.93). [score:5]
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89
[+] score: 5
In the 3′ untranslated region (UTR), conflicting results were reported concerning association of HLA-G expression and the ex8 ins/ del polymorphism (16); the 3142G allele was identified as a binding site for the microRNA-152 family (17) and 3187A/G and 3196C/G were reported to influence mRNA stability. [score:5]
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90
[+] score: 5
Lin et al. found robust and significant downregulation of 8 miRNAs in the hypertonic dialysate group (miR-31, miR-93, miR-100, miR-152, miR-497, miR-192, miR-194, and miR-200b) and increased expression of miR-122 was observed in the hypertonic dialysate group compared with the saline and control groups [26]. [score:5]
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91
[+] score: 5
McBride et al. (2012) observed nine miRNAs (miR-125a, miR-199a-3p, miR-125b, miR-99a, let-7c, miR-145, miR-31, miR-202 and miR-27b) with decreased expression and eight miRNAs (miR-503, miR-21, miR-29b, miR-142-3p, miR-34a, miR-152, miR-25 and miR-130a) with increased expression between the follicular and luteal stages in ovine ovarian tissues [21]. [score:5]
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92
[+] score: 4
Theodore SC MicroRNA profiling of novel African American and Caucasian prostate cancer cell lines reveals a reciprocal regulatory relationship of miR-152 and DNA methyltransferase 1Oncotarget. [score:4]
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93
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MiR-8 [20], miR152 [21], miR124 [22] and miR-376c [23] have been reported to regulate the expression of TGFα. [score:4]
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94
[+] score: 4
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-16-1, hsa-mir-21, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-29a, hsa-mir-30a, hsa-mir-31, hsa-mir-32, hsa-mir-33a, hsa-mir-96, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-16-2, hsa-mir-192, hsa-mir-199a-1, hsa-mir-148a, hsa-mir-30c-2, hsa-mir-10a, hsa-mir-10b, hsa-mir-34a, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-182, hsa-mir-183, hsa-mir-199a-2, hsa-mir-199b, hsa-mir-203a, hsa-mir-204, hsa-mir-211, hsa-mir-212, hsa-mir-181a-1, hsa-mir-214, hsa-mir-217, hsa-let-7g, hsa-let-7i, hsa-mir-15b, hsa-mir-27b, hsa-mir-122, hsa-mir-125b-1, hsa-mir-132, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-137, hsa-mir-138-2, hsa-mir-145, hsa-mir-153-1, hsa-mir-153-2, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125b-2, hsa-mir-126, hsa-mir-127, hsa-mir-136, hsa-mir-138-1, hsa-mir-146a, hsa-mir-150, hsa-mir-185, hsa-mir-193a, hsa-mir-194-1, hsa-mir-320a, hsa-mir-155, hsa-mir-181b-2, hsa-mir-194-2, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-200a, hsa-mir-34c, hsa-mir-26a-2, hsa-mir-302b, hsa-mir-369, hsa-mir-375, hsa-mir-378a, hsa-mir-328, hsa-mir-335, hsa-mir-133b, hsa-mir-409, hsa-mir-484, hsa-mir-485, hsa-mir-486-1, hsa-mir-490, hsa-mir-495, hsa-mir-193b, hsa-mir-497, hsa-mir-512-1, hsa-mir-512-2, hsa-mir-506, hsa-mir-509-1, hsa-mir-532, hsa-mir-92b, hsa-mir-548a-1, hsa-mir-548b, hsa-mir-548a-2, hsa-mir-548a-3, hsa-mir-548c, hsa-mir-33b, hsa-mir-548d-1, hsa-mir-548d-2, hsa-mir-1224, hsa-mir-320b-1, hsa-mir-320c-1, hsa-mir-320b-2, hsa-mir-378d-2, hsa-mir-802, hsa-mir-509-2, hsa-mir-509-3, hsa-mir-548e, hsa-mir-548j, hsa-mir-548k, hsa-mir-548l, hsa-mir-548f-1, hsa-mir-548f-2, hsa-mir-548f-3, hsa-mir-548f-4, hsa-mir-548f-5, hsa-mir-548g, hsa-mir-548n, hsa-mir-548m, hsa-mir-548o, hsa-mir-548h-1, hsa-mir-548h-2, hsa-mir-548h-3, hsa-mir-548h-4, hsa-mir-548p, hsa-mir-548i-1, hsa-mir-548i-2, hsa-mir-548i-3, hsa-mir-548i-4, hsa-mir-320d-1, hsa-mir-320c-2, hsa-mir-320d-2, hsa-mir-548q, hsa-mir-548s, hsa-mir-378b, hsa-mir-548t, hsa-mir-548u, hsa-mir-548v, hsa-mir-548w, hsa-mir-320e, hsa-mir-548x, hsa-mir-378c, hsa-mir-4262, hsa-mir-548y, hsa-mir-548z, hsa-mir-548aa-1, hsa-mir-548aa-2, hsa-mir-548o-2, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-548h-5, hsa-mir-548ab, hsa-mir-378f, hsa-mir-378g, hsa-mir-548ac, hsa-mir-548ad, hsa-mir-548ae-1, hsa-mir-548ae-2, hsa-mir-548ag-1, hsa-mir-548ag-2, hsa-mir-548ah, hsa-mir-378h, hsa-mir-548ai, hsa-mir-548aj-1, hsa-mir-548aj-2, hsa-mir-548x-2, hsa-mir-548ak, hsa-mir-548al, hsa-mir-378i, hsa-mir-548am, hsa-mir-548an, hsa-mir-203b, hsa-mir-548ao, hsa-mir-548ap, hsa-mir-548aq, hsa-mir-548ar, hsa-mir-548as, hsa-mir-548at, hsa-mir-548au, hsa-mir-548av, hsa-mir-548aw, hsa-mir-548ax, hsa-mir-378j, hsa-mir-548ay, hsa-mir-548az, hsa-mir-486-2, hsa-mir-548ba, hsa-mir-548bb, hsa-mir-548bc
Prenatal ethanol exposure was also shown to up-regulate several microRNAs (miR-9, miR-10a, miR-10b, miR-30a-3p, miR-145, and miR-152) in the fetal brain [139]. [score:4]
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95
[+] score: 4
By regression analysis adjusting for age, sex, and multiple testing we found 12 miRNAs (miR-152, miR-30a-5p, miR-181a, miR-24, miR-148a, miR-210, miR-27a, miR-29a, miR-26a, miR-27b, miR-25, and miR-200a) to be significantly differentially expressed between either both diabetes cohorts and the control group or just one of the diabetes cohorts and the controls (Table 1) (P < 0.05). [score:3]
Even more importantly we found quite a few miRNAs with yet unidentified function related to T1D as miR-152 and miR-30a-5p. [score:1]
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96
[+] score: 4
Significantly-expressed miNRAs Scope Sample Technique Normalization let-7c, miR-152 (down) 120 NSCLCs vs. [score:3]
Decreased plasma let-7c and miR-152 as noninvasive biomarker for non-small-cell lung cancer. [score:1]
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97
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Their expressions were not altered in WT mice, with the exception of miR-152, which was consistently lower than that in non-colitic IL10 [−/−] mice. [score:3]
Based on this, miRNA-152 was excluded from the signature. [score:1]
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98
[+] score: 4
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-mir-15a, hsa-mir-18a, hsa-mir-33a, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-107, mmu-mir-27b, mmu-mir-126a, mmu-mir-128-1, mmu-mir-140, mmu-mir-146a, mmu-mir-152, mmu-mir-155, mmu-mir-191, hsa-mir-10a, hsa-mir-211, hsa-mir-218-1, hsa-mir-218-2, mmu-mir-297a-1, mmu-mir-297a-2, hsa-mir-27b, hsa-mir-128-1, hsa-mir-140, hsa-mir-191, hsa-mir-126, hsa-mir-146a, mmu-let-7a-1, mmu-let-7a-2, mmu-mir-15a, mmu-mir-18a, mmu-mir-103-1, mmu-mir-103-2, mmu-mir-342, hsa-mir-155, mmu-mir-107, mmu-mir-10a, mmu-mir-218-1, mmu-mir-218-2, mmu-mir-33, mmu-mir-211, hsa-mir-374a, hsa-mir-342, gga-mir-33-1, gga-let-7a-3, gga-mir-155, gga-mir-18a, gga-mir-15a, gga-mir-218-1, gga-mir-103-2, gga-mir-107, gga-mir-128-1, gga-mir-140, gga-let-7a-1, gga-mir-146a, gga-mir-103-1, gga-mir-218-2, gga-mir-126, gga-let-7a-2, gga-mir-27b, mmu-mir-466a, mmu-mir-467a-1, hsa-mir-499a, hsa-mir-545, hsa-mir-593, hsa-mir-600, hsa-mir-33b, gga-mir-499, gga-mir-211, gga-mir-466, mmu-mir-675, mmu-mir-677, mmu-mir-467b, mmu-mir-297b, mmu-mir-499, mmu-mir-717, hsa-mir-675, mmu-mir-297a-3, mmu-mir-297a-4, mmu-mir-297c, mmu-mir-466b-1, mmu-mir-466b-2, mmu-mir-466b-3, mmu-mir-466c-1, mmu-mir-466e, mmu-mir-466f-1, mmu-mir-466f-2, mmu-mir-466f-3, mmu-mir-466g, mmu-mir-466h, mmu-mir-467c, mmu-mir-467d, mmu-mir-466d, hsa-mir-297, mmu-mir-467e, mmu-mir-466l, mmu-mir-466i, mmu-mir-466f-4, mmu-mir-466k, mmu-mir-467f, mmu-mir-466j, mmu-mir-467g, mmu-mir-467h, hsa-mir-664a, hsa-mir-1306, hsa-mir-1307, gga-mir-1306, hsa-mir-103b-1, hsa-mir-103b-2, gga-mir-10a, mmu-mir-1306, mmu-mir-3064, mmu-mir-466m, mmu-mir-466o, mmu-mir-467a-2, mmu-mir-467a-3, mmu-mir-466c-2, mmu-mir-467a-4, mmu-mir-466b-4, mmu-mir-467a-5, mmu-mir-466b-5, mmu-mir-467a-6, mmu-mir-466b-6, mmu-mir-467a-7, mmu-mir-466b-7, mmu-mir-467a-8, mmu-mir-467a-9, mmu-mir-467a-10, mmu-mir-466p, mmu-mir-466n, mmu-mir-466b-8, hsa-mir-466, hsa-mir-3173, hsa-mir-3618, hsa-mir-3064, hsa-mir-499b, mmu-mir-466q, hsa-mir-664b, gga-mir-3064, mmu-mir-126b, gga-mir-33-2, mmu-mir-3618, mmu-mir-466c-3, gga-mir-191
Previous studies revealed that five miRNA genes as well as their host genes (hsa-mir-10a/ HOXB4, hsa-mir-126/ EGFL7, hsa-mir-152/ COPZ2, hsa-mir-191/ DALRD3, and hsa-mir-342/ EVL) were found to be epigenetically downregulated, either by histone modification and/or CpG island hypermethylation in the promoter region in cancer cells [27], [86]– [89] (Table 2 ). [score:4]
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99
[+] score: 4
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-16-1, hsa-mir-17, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-20a, hsa-mir-21, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-29a, hsa-mir-30a, hsa-mir-98, hsa-mir-101-1, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-106a, hsa-mir-16-2, hsa-mir-192, hsa-mir-148a, hsa-mir-30c-2, hsa-mir-30d, hsa-mir-7-1, hsa-mir-7-2, hsa-mir-7-3, hsa-mir-10a, hsa-mir-10b, hsa-mir-34a, hsa-mir-210, hsa-mir-215, hsa-mir-200b, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-30b, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-125b-1, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-137, hsa-mir-138-2, hsa-mir-143, hsa-mir-144, hsa-mir-145, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-126, hsa-mir-127, hsa-mir-138-1, hsa-mir-146a, hsa-mir-193a, hsa-mir-194-1, hsa-mir-206, hsa-mir-320a, hsa-mir-200c, hsa-mir-1-1, hsa-mir-155, hsa-mir-194-2, hsa-mir-106b, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-200a, hsa-mir-302a, hsa-mir-101-2, hsa-mir-34b, hsa-mir-34c, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-302b, hsa-mir-302c, hsa-mir-302d, hsa-mir-369, hsa-mir-371a, hsa-mir-340, hsa-mir-335, hsa-mir-133b, hsa-mir-146b, hsa-mir-519e, hsa-mir-519c, hsa-mir-519b, hsa-mir-519d, hsa-mir-519a-1, hsa-mir-519a-2, hsa-mir-499a, hsa-mir-504, hsa-mir-421, hsa-mir-320b-1, hsa-mir-320c-1, hsa-mir-320b-2, hsa-mir-190b, hsa-mir-301b, hsa-mir-302e, hsa-mir-302f, hsa-mir-320d-1, hsa-mir-320c-2, hsa-mir-320d-2, hsa-mir-320e, hsa-mir-371b, hsa-mir-499b
The miR-29 gene family directly targets the global DNA methyltransferases DNMT3A and DNMT3B in lung cancer cells [42], as do miR-143, miR-148a and miR-152 in in colorectal cancer, malignant cholangiocytes or hepititis B induced hepatocellular carcinoma cells [43, 44, 45]. [score:4]
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100
[+] score: 4
In addition, miR-152 is down regulated in both mouse and human neuroblastoma, having a documented tumor suppressor function in human neuroblastoma [38]. [score:4]
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