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46 publications mentioning hsa-mir-489

Open access articles that are associated with the species Homo sapiens and mention the gene name mir-489. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 520
In this study, we identified miR-489 as one of the candidate miRNAs whose expression was downregulated by HER2 downstream MAPK signaling and for the first time showed that miR-489 directly binds to the 3′-UTR of HER2 mRNA and down-regulates its expression. [score:12]
Among many deregulated miRNAs in HER2 -overexpressing breast cancer cells, miR-489 expression may be directly regulated by HER2 signaling since treatment with HER2/EGFR dual inhibitor lapatibnib can significantly reverse miR-489 expression status in HER2 -positive breast cancer cells. [score:12]
F. General feedback loop mo del proposed by the study, where HER2 signaling through SHP2 and ERK promotes cell proliferation and inhibits miR-489 expression, whereas miR-489 downregulates both HER2 and SHP2 directly to inhibit cell proliferation. [score:11]
Although our clinical data shows that miR-489 expression is lower in HER2 -positive tumors, its expression can be downregulated in many human breast cancers independent of their HER2 expression status. [score:10]
C. Colony formation assay on MCF7 and MDA-MB231 cells transfected with either scramble, mimic miR-489 or inhibitor mir-489 * p<0.05, ** p value < 0.01. miR-489 regulates HER2 signaling pathway by directly targeting HER2 and its downstream gene Shp2According to the miRwalk pathway target prediction, HER2 pathway can be potentially targeted by miR-489. [score:10]
Over expression of miR-489 inhibits tumor growth in vivoSince miR-489 inhibited cell proliferation and decreased transforming capacity of cells to form colonies in vitro (Figure 3C), we wanted to assess its ability to inhibit tumor growth in vivo. [score:9]
Since p-ERK levels were also inversely correlated with the expression of miR-489, we hypothesized that miR-489 affects ERK signaling by downregulating the expression of HER2 and SHP2. [score:8]
Given that the expression levels of miR-489 is strongly correlated with tumor aggressive phenotypes, it raises the possibility that targeting miR-489 as a therapy may be of benefit not just in HER2/ neu -overexpressing tumors, but also in a broader subsets of patients. [score:7]
Together, our results strongly suggested that miR-489 may directly target HER2 and SHP2 in breast cancer cells and regulate its expression. [score:7]
Previous studies showed that miR-489 can downregulate SHP2 expression in hypopharyngeal squamous cell carcinomas by directly binding to its 3′UTR[18]. [score:7]
Overexpression of miR-489 inhibited cell growth and invasion and epithelial-to-mesenchymal transition (EMT) properties by targeting several genes including Shp2, Smad3, Akt3 and Suz12. [score:7]
These results overall allow us to create a double feedback loop mo del where HER2 and SHP2 activates ERK signaling which results in the inhibition of miR-489 expression, while miR-489 targets both SHP2 and HER2 simultaneously to affect the ERK signaling and therefore decrease the cell proliferation (Figure 4F). [score:7]
We have also confirmed that miR-489 can directly downregulate SHP2 expression in breast cancer cells. [score:7]
Next, to determine the role of a particular signaling pathway in miR-489 transcriptional regulation, MCF7 HER2 cells were treated with the HER2-downstream signaling pathways inhibitors targeting NF-κB (Bay-11-7082), PI3K (LY294002), AKT1 (SC-66), MEK (U0126), MAPK (PD0325901), SRC (PP2), p38 (SB-203580), and STAT3 (Stattic) signaling. [score:6]
First, overexpression of miR489 results in down-regulation of HER2 in several breast cancer cell lines. [score:6]
These results clearly demonstrated that miR-489 inhibits HER2 expression by directly binding to its 3′UTR region. [score:6]
Our results clearly indicated that miR-489 over expression inhibited cell proliferation in all of the four tested breast cancer cell lines and conversely, knockdown of miR-489 increased cell proliferation (Figure 3A). [score:6]
The expression of miR-489 is downregulated in hypopharyngeal squamous cell carcinoma (HSCC), non-small cell lung cancer (NSCLC) and in breast cancer [18, 19]. [score:6]
Overall, these data suggest that dysregulation of miR-489 may contribute to tumor development and affect the sensitivity to anti-cancer drugs by regulating different target genes in a context -dependent manner. [score:6]
Our data demonstrated that expression of CALCR mRNA, pre-miR-489 and mature miR-489 are down regulated to a similar extent (Figure 2A), suggesting that expression of miR-489 may be controlled at the transcription level. [score:6]
Expression of miR-489 is downregulated at transcriptional level by HER2 signaling. [score:6]
However, expression of miR-489 was rescued only by si-SHC knockdown and not by AKT1 knockdown. [score:5]
miR-489 regulates HER2 signaling pathway by directly targeting HER2 and its downstream gene Shp2. [score:5]
Taken together, increased expression of miR-489 in breast cancer cells resulted into inhibited cell proliferation and transformation. [score:5]
C. Effects of HER2-downstream signaling inhibitor treatments on the expression of miR-489 in MCF-7 HER2 cells. [score:5]
Protein expression data was quantified and correlated with the expression of miR-489 in each cell line. [score:5]
Moreover, we also observed that expression of total HER2 and SHP2 were reduced in miR-489 mimic transfected cells and elevated in the miR-489 inhibitor transfected cells (Figure 4A). [score:5]
To further validate that miR-489 might be regulated by MEK-ERK signaling possibly through HER2 down-regulation, we treated cells with si-AKT1 and si-SHC to block two downstream effectors of HER2 signaling. [score:5]
It should also be kept in mind that besides HER2, miR-489 may target many other target genes as well. [score:5]
HER2 expression is associated with higher cell proliferation, whereas miR-489 expression may be associated with slow proliferation or quiescent status [17]. [score:5]
Moreover, our clinical data analysis indicated that miR-489 expression was significantly downregulated in tumor tissues compared to the normal breast tissues from same patients. [score:5]
The qRT-PCR indicated that miR-489 levels were most significantly rescued by two inhibitors, both targeting the MEK-ERK signaling (Figure 2C). [score:5]
Since miR-489 inhibited cell proliferation and decreased transforming capacity of cells to form colonies in vitro (Figure 3C), we wanted to assess its ability to inhibit tumor growth in vivo. [score:5]
Our qRT-PCR data demonstrated that miR-489, miR-125b and miR-99a at least partially restored their expression profile after inhibition of HER2 phosphorylation (Figure 1C). [score:5]
Thirdly, the expression levels of miR-489 is inversely correlated with HER2 expression status in clinical breast cancer samples. [score:5]
The close association of miR-489 expression with clinical parameters implicates miR-489 can be a new prognostic marker and potential therapeutic target for breast cancer. [score:5]
To find whether HER2 affects the expression of miR-489 at transcriptional level, we quantified the expression levels of mature miR-489, pre-miR-489 and CALCR mRNA in MCF7 vect and HER2 cells using qRT-PCR (Figure 2A). [score:5]
Among different miRNAs, miR-489 stood out, as its overexpression inhibited cell growth in all cell lines examined [18]. [score:5]
Loss of miR-489 expression in HER2 -positive breast cancer cells suggests that miR-489 might have tumor suppressive function. [score:5]
To demonstrate the effect of SHP2 or HER2 OE on cell survival against miR-489, SHP2 and HER2 -overexpressing MDA-MB-231 cells were transfected with either mimic or inhibitor of miR-489. [score:5]
We confirmed that overexpression of miR-489 reduced SHP2 expression in breast cancer cell lines at both mRNA and protein levels (Supplementary Figure S4). [score:5]
Consistently, we show that restoration of miR-489 in HER2 -overexpressing breast cancer cells strongly inhibits cell proliferation both in vitro and in vivo. [score:5]
As expected, patients with low miR-489 expression had a relatively poor overall survival than those with high miR-489 expression (Figure 6D). [score:5]
For the mutation analysis putative miR-489 target site within 3′UTR of HER2 was mutated by Phusion site directed mutagenesis kit (Thermofisher Cat# F-541). [score:5]
According to the miRwalk pathway target prediction, HER2 pathway can be potentially targeted by miR-489. [score:5]
Overexpression of miR-489 inhibits tumor growth in vivo. [score:5]
Overexpression of miR-489 inhibits cell growth in vitro. [score:5]
Overexpression of miR-489 in breast cancer cells inhibits cell proliferation. [score:5]
Over expression of miR-489 inhibits tumor growth in vivo. [score:5]
Because miR-489 is mainly regulated via the MEK-ERK pathway which can be activated by many overexpressing oncogenes or receptors or cytokines. [score:4]
miR-489 targets HER2 signaling pathway by directly binding the 3′ UTR of HER2. [score:4]
Overexpression of miR-489 inhibits cell growth in vitroTo explore the biological function of miR-489 in breast cancer, we transiently transfected breast cancer cells with miR-489 mimic or inhibitor and measured cell growth by MTT assay. [score:4]
Previous studies have validated one of the downstream effector of HER2 signaling SHP-2 as the direct target of miR-489 [18, 27]. [score:4]
Next, to examine whether miR-489 inhibits colony formation ability of cancer cells, both MCF7 and MDA-MB-231 cells transfected with either the scramble, mimic or miR-489 inhibitor were used to perform colony formation assay. [score:4]
For example, miR-489 has been shown to directly target other oncogenes such as Shp2 in HSCC [18], SMAD3 in breast cancer [19], AKT3 in ovarian cancer [36] and Dek in mouse muscle stem cells [17, 36]. [score:4]
Overall, these results clearly demonstrated that miR-489 expression is transcriptionally regulated mainly by the HER2 -driven MAPK downstream signaling. [score:4]
A. MTT cell viability assay showing the rate of cell proliferation of MCF7-Vect and HER2, BT-474, T47D and MDA-MB-231 cells transfected with miR-489 mimic or inhibitor for 72 h. B. Cell cycle analysis of cells transfected with miR-489 mimic and inhibitor using FACS. [score:4]
Figure 3 A. MTT cell viability assay showing the rate of cell proliferation of MCF7-Vect and HER2, BT-474, T47D and MDA-MB-231 cells transfected with miR-489 mimic or inhibitor for 72 h. B. Cell cycle analysis of cells transfected with miR-489 mimic and inhibitor using FACS. [score:4]
This data indicated that miR-489 may be directly or indirectly involved in regulating cell cycle progression. [score:4]
Together, these data demonstrated that miR-489 delivered through nanoparticles inhibits tumor growth in xenografts by decreasing cell proliferation at least partially by blocking the HER2-, SHP2-MAPK signaling axis. [score:3]
Unlike many tumor suppressors that normally induce cell cycle arrest and apoptosis, miR-489 dramatically reduced ki-67 positive population, but didn't induce apoptosis. [score:3]
Loss of miR-489 expression is especially associated with tumor in higher grades and higher stages (Supplementary Table S2). [score:3]
Figure 4 A. Effects of miR-489 and inhibitor treatment on HER2-downstream signaling. [score:3]
Conversely, transfection of miR-489 inhibitor can further increase cell proliferation rate which is evidenced by increase cell population in S phase. [score:3]
Treatment of cells with increased concentration of nanoparticle resulted in a decrease in HER2 expression levels in a dose -dependent manner (Supplementary Figure S4B), indicating that nanoparticles can effectively deliver miR-489 into tumor cells. [score:3]
B. Western blot analysis of other breast cancer cell lines treated with miR-489 mimic also showed reduction in HER2 expression. [score:3]
In addition, multivariate analysis revealed that miR-489 expression was an independent prognostic factor to predict overall patient survival (Table 1). [score:3]
Furthermore, we analyzed the correlation between miR-489 expression level and other clinical parameters including overall survival, HER2 status, metastasis, grade and stages (Supplementary Table S2). [score:3]
We also confirmed that miR-489 can target another HER2 downstream gene Shp2 in breast cancer cells. [score:3]
To further validate that loss of miR-489 expression in breast cancer epithelial cells, we did in situ fluorescent hybridization on breast cancer tissue and adjacent normal tissues. [score:3]
Previously, it was already known that miR-489 functions as a tumor suppressor gene in hypopharygeal squamous cell carcinoma (HSCC)[18]. [score:3]
In a complementary experiment, transient transfection of miR-489 inhibitor can increase the protein levels of HER2. [score:3]
High levels of miR-489 expression were detected in normal epithelial cells and occasionally myoepithelial cells, however, the staining signal intensities were weak in the stromal and tumor areas (Figure 6B). [score:3]
We found that there is an inverse correlation between the expression of miR-489 and HER2 in clinical samples as indicated by our in vitro data. [score:3]
To verify whether miR-489 has any effect on HER2 signaling, we transfected MCF7 Vect and HER2 cells with mimic or inhibitor of miR-489 and total protein was isolated after 72 h. Western blotting analysis was performed to examine the HER2 signaling in the transfected cells (Figure 4A). [score:3]
Indeed, we observed a dramatic decrease or increase in the S phase population of miR-489 mimic or miR-489 inhibitor transfected cells respectively (Figure 3B). [score:3]
E. Effects of siRNA -mediated blockage of AKT and MAPK signaling on the expression of miR-489. [score:3]
In addition, loss of miR-489 expression confer tumor cells resistance to chemotherapeutic drugs [20]. [score:3]
MCF7 HER2 cells were co -transfected with either of these vectors with miR-489 expressing vector or empty vector and renilla expressing vector for 48 h. Firefly luciferase was measured for each condition and normalized with renilla luciferase. [score:3]
It remains unknown whether the expression ratio of HER2/miR-489 determines the overall cell proliferation rate of a tumor or tumor heterogeneity with mixed cell population with high/slow proliferation rates. [score:3]
In addition, miR-489 seems to play a tumor suppressive role in a few different types of cancers. [score:3]
This may explain why miR-489 is broadly down-regulated in breast cancer cells compared to their adjacent normal tissues, especially in HER2 -positive and basal subtypes of breast cancers. [score:3]
Multivariate cox proportional hazard regression mo del of the risk of overall survival according to miR-489 expression adjusted for clinic-pathological factors. [score:3]
Identification of HER2 as a new target in breast cancer cells may shed light on the function of miR-489 in breast tumorigenesis. [score:3]
One could envisage that miR-489 can dramatically modulate HER2 signaling networks via simultaneously targeting multiple downstream genes during breast carcinogenesis. [score:3]
The patient samples were stratified into three equal groups based on the expression levels of miR-489. [score:3]
Low expression of miR-489 in primary breast cancer is associated with aggressive phenotypes and poor clinical outcomes. [score:3]
Figure 5 A. Nanoparticle- delivered miR-489 inhibits tumor growth. [score:3]
Conversely, cells transfected with inhibitor of miR-489, as predicted had opposite effect and resulted in forming more colonies than the cells transfected with scramble miRNA. [score:3]
To explore the clinical relevance of miR-489 expression in breast cancer, we performed quantitative RT-PCR analysis of cDNAs generated from 11 pairs of breast cancer and their corresponding adjacent normal tissue. [score:3]
B. FISH analysis of miR-489 expression in normal breast tissue and adjacent tumor tissues. [score:3]
In this study, we for the first time demonstrated that HER2 is a bona fide target of miR-489 by the following evidences. [score:3]
Expression status of miR-489 in primary breast cancer tissues. [score:3]
A. Effects of miR-489 and inhibitor treatment on HER2-downstream signaling. [score:3]
Understanding the signaling cross-talk between miR-489 and HER2 indicate that the HER2-SHP2-MAPK signaling axis and miR-489 form a double -negative regulation loop to regulate cell proliferation in breast cancer (Figure 4F). [score:3]
Consistently, overexpression of miR-489 appeared not to induce apoptosis, which is evident by slight changes in the Sub-G [0] cell populations. [score:3]
The strong positive correlation between the expression levels of CALCR and miR-489 in clinical samples further confirmed this conclusion (Figure 2B). [score:3]
A. Nanoparticle- delivered miR-489 inhibits tumor growth. [score:3]
D. Expression status of miR-489 predicts clinical outcome. [score:3]
Moreover, our IHC data also revealed that HER2 and SHP2 expression was lower in miR-489 injected tumors compared to the tumors injected with scramble (Figure 5B). [score:2]
Conversely, miR-489 inhibitor transfected cells exhibited a reversed effect on HER2 signaling compared to miR-489 mimic. [score:2]
Our MTT data indicated that both SHP2 and HER2 overexpression led to the increased cell survival significantly when compared to the vector control cells in the presence of miR-489 mimic (Figure 4E). [score:2]
E. MTT assay showing relative cell survival of vector control, SHP2 OE or HER2 OE cells transfected with scramble, mimic miR-489 or inhibitor miR-489 **, p<0.01; *, p<0.05. [score:2]
C. Colony formation assay on MCF7 and MDA-MB231 cells transfected with either scramble, mimic miR-489 or inhibitor mir-489 * p<0.05, ** p value < 0.01. [score:2]
Here, it is likely that the HER2-SHP2-MAPK/miR-489 feedback loop is involved in regulation of quiescence/proliferation phenotypical transition in cancer cells. [score:2]
To test the possibility that miR-489 may regulate cell cycle progression, we examined the cell cycle profiles by FACS analysis. [score:2]
Therefore, the HER2-SHP2-MAPK and miR-489 signaling pathways form a double negative feedback loop which regulates breast cancer cell proliferation both in vitro and in vivo. [score:2]
We also found that the expression levels of miR-489 tend to be lower in HER2 -positive and basal subtypes compared to both luminal and normal-like subtypes of breast cancer (Figure 6C). [score:2]
These results led us to believe that MEK-ERK signaling might be crucial in controlling the miR-489 transcription, although STAT3 and SRC pathways may also be involved in its regulation. [score:2]
HER2 negatively regulates miR-489 mainly via the MAPK pathway. [score:2]
A few recent studies have shown that miR-489 plays an important role in both development and tumorigenesis. [score:2]
Consistently, our data showed that the expression levels of miR-489 are lower in basal-like and HER2 -positive subtypes compared to luminal subtypes of breast cancers. [score:2]
Furthermore, to understand triggering of which pathway results in miR-489 down regulation, we isolated proteins from 13 breast cancer cell lines and performed western blotting for p-ERK and pAKT (Supplementary Figure S2). [score:2]
A. Real-time PCR analysis ofcalcitonin receptor (CALCR) mRNA, pre-miR-489 and mature miR-489 RNA levels in MCF7-HER2 and MCF7-vect cells. [score:1]
After the tumors were palpable, all 7 tumor sites were injected with miR-489 or scramble miRNA encapsulated in nanoparticle every three times. [score:1]
The nanoparticle packaged with miR-489 showed similar size distribution as control nanoparticles (Supplementary Figure S4A). [score:1]
F. Pearson analysis of theCorrelation between p-AKT or p-ERK1/2 and mature miR-489 in breast cancer lines. [score:1]
The statistical data clearly demonstrated that p-ERK, not p-AKT, was negatively correlated with the levels of miR-489 in all 13 breast cancer cell lines (Figure 2F). [score:1]
B. IHC analysis of cells in tumors treated with nanoparticle- delivered miR-489 or scrambled miRNA for HER2, SHP2, p-ERK and Ki-67. [score:1]
A. Real-time RT-PCR analysis of miR-489 in breast cancer tumor tissues and their adjacent normal tissues from 11 breast cancer patients. [score:1]
Our data showed that in the presence of miR-489, luciferase activity of wt HER2 3′UTR and not the mutant HER2 3′UTR is significantly reduced (Figure 4C). [score:1]
The linear correlations between CALCR and miR-489 ligand expression in primary breast cancer tissues were evaluated with Pearson correlation coefficient analysisusing public dataset [51]. [score:1]
Given that the expression statuses of miR-489 tend to be associated with the aggressive subtypes of breast cancers, we performed the Kaplan-Meier survival analysis to further evaluate the prognostic value. [score:1]
Univariate regression analysis and multivariate Cox PH regression analysis were performed to demonstrate the correlation between the patient survival and miR-489 while accounting for other potential predictors (covariates). [score:1]
The clinical effect of the gene expression profiles of miR-489 was further evaluated using two published datasets: Dvinge et al, 1302 breast cancer patients [51], and Rinaldis et al, 181 breast cancer patients [52]. [score:1]
By searching through 3′UTR sequence of HER2, we identified a potential partially complementary miR-489 binding site. [score:1]
Given that a double -negative feedback loop generally allows the maintenance of bi-stable states, we tend to believe that the ratio of HER2/miR-489 is critical for generation of tumor heterogeneity and determination of tumor behaviors. [score:1]
In a previous screening for microRNAs, which are essential for HER2 positive breast cancer cell growth, miR-489 has been identified as one of the potential candidates to attenuate HER2 signaling, but the underlying mechanism remains unknown [35]. [score:1]
Figure 6 A. Real-time RT-PCR analysis of miR-489 in breast cancer tumor tissues and their adjacent normal tissues from 11 breast cancer patients. [score:1]
Cheung et al. has shown that the miR-489 pathway is essential for the maintenance of the quiescent state of muscle stem cells [17]. [score:1]
Secondly, a putative miR-489 binding site is identified in the 3′UTR of HER2 mRNA. [score:1]
We decided to focus further on the function of miR-489 given that very little is known about its function in breast cancer. [score:1]
Our results indicated that miR-489 mimic dramatically impaired HER2 signaling as evident by reduced HER2, phospho- HER2, SHP2, phospho-AKT and phospho-ERK (Figure 4A). [score:1]
Figure 2 A. Real-time PCR analysis ofcalcitonin receptor (CALCR) mRNA, pre-miR-489 and mature miR-489 RNA levels in MCF7-HER2 and MCF7-vect cells. [score:1]
To explore the possibility to use miR-489 for therapy, we developed a nanoparticle delivery system to deliver miR-489 into tumor cells. [score:1]
C. Graph showing number of Ki-67 positive cells intumors treated with nanoparticle- delivered miR-489 or scrambled miRNA. [score:1]
The linear correlations between CALCR and miR-489 ligand expression in primary breast cancer tissues were evaluated with Pearson correlation coefficient analysis. [score:1]
Together, our results support that miR-489 can be serve as a prognostic marker in breast cancer and loss of miR-489 in breast cancer may contribute to tumor progression. [score:1]
LNA-substituted DNA oligonucleotide probe for miR-489 was obtained from Exiqon (Cat#38599-01) labelled with digoxigenin at the 5′ terminus. [score:1]
Preparation of miR-489- delivering nanoparticle. [score:1]
C. A schematic representation of the HER2 mRNA with putative miR-489 binding site in the 3′ UTR, where the seed region is highlighted. [score:1]
The miR-489 gene sequence is located in the intronic region of calcitonin receptor (CALCR) gene (Supplementary Figure S1). [score:1]
B. Correlation between CALCR mRNA and mature miR-489 in clinical breast cancer tissue. [score:1]
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[+] score: 325
Other miRNAs from this paper: hsa-mir-381, mmu-mir-381, mmu-mir-489
Interestingly, miR-489 overexpression in HCT116 cells resulted in up-regulation of epithelial marker (E-cadherin) and down-regulation of mesenchymal marker (Vimentin) as well as the morphology of epithelial-like cells (Figure 4A). [score:9]
As expected, re -expression of TWIST1 abrogated the inhibitory effect of miR-489 on EMT process with decreased expression of E-cadherin and increased expression of Vimentin in HCT116 cells (Figure 7A). [score:9]
and IF analysis indicated the miR-489 overexpression up-regulated E-cadherin while down-regulated Vimentin. [score:9]
Recently, the expression miR-489 is found to be down-regulated in HCC tissues, especially in early recurrent cases, and miR-489 underexpression contributes to migration and invasion of HCC cells [20, 31]. [score:8]
Furthermore, miR-489 functions as a tumor suppressor in hypopharyngeal squamous cell carcinoma and suppresses growth of cancer cells by targeting protein tyrosine phosphatase, non-receptor type 11 (PTPN11) [17]. [score:7]
Notably, survival analysis indicated miR-489 low expressing CRC patients showed a obvious reduced overall survival and disease-free survival compared to miR-489 high expressing cases (P < 0.05, respectively, Figure 1C and 1D). [score:6]
miR-489 low expressing CRC patients showed a significant decreased overall survival and disease-free survival compared to miR-489 high expressing cases. [score:6]
Next, we demonstrated that CHRF inversely regulated miR-489 expression and promotes TWIST1 expression and EMT progression in CRC cells. [score:6]
However, miR-489 is prominently upregulated in oral squamous cell carcinoma [21], clear cell renal cell carcinoma [22, 23], suggesting that the expression and role of miR-489 are variability in different cancers. [score:6]
Precursor miR-489 (HmiR0107-MR04), miR-489 inhibitors (HmiR-AN0528-AM04), and corresponding scrambled control clones (CmiR0001-MR04; CmiR-AN0001-AM04) were purchased, and CHRF siRNA, CHRF expression vector and matched scrambled control vectors were synthesized and purchased from GeneCopoeia [™] (Guangzhou, China). [score:5]
CRC patients were divided into miR-489 high expression group and miR-489 low expression group according to the cutoff value, which was defined as the median level of miR-489. [score:5]
Thus, to disclose the potential molecular mechanisms involved in the role of miR-489 in CRC cells, we searched for candidate target genes of miR-489 using publicly available databases, including TargetScan and miRanda. [score:5]
Hence, these results further confirmed that miR-489 inhibits migration, invasion and EMT process of CRC cells probably by targeting TWIST1. [score:5]
In addition, miR-489 overexpression suppressed the invasive ability of HCT116 cells in vitro (P < 0.05, Figure 2C). [score:5]
miR-489 overexpression inhibits liver metastasis of CRC in nude mice. [score:5]
Thus, miR-489 inhibits metastasis and EMT of CRC cells probably via targeting TWIST1. [score:5]
Figure 7(A) miR-489 overexpressing HCT116 cells were transfected with TWIST1 expression vector. [score:5]
miR-489 directly targets and regulates TWIST1 in CRC cells. [score:5]
TWIST1 overexpression abrogated the inhibitory effects of miR-489 on EMT process. [score:5]
While, miR-489 loss in SW480 cells decreased E-cadherin expression and increased Vimentin expression, and then led to the morphology of mesenchymal-like cells (Figure 4B). [score:5]
In addition, the expressions of miR-489 in five CRC cell lines (HCT116, Caco2, HT29, SW620, SW480) were notably down-regulated compared to a human intestinal epithelial cell line (HIEC) (P < 0.05, respectively, Figure 1B). [score:5]
Moreover, miR-489 regulates ovarian cancer cell survival, growth and apoptosis via suppression of Akt3 [18]. [score:4]
Thus, TWIST1 is a direct target of miR-489 in CRC. [score:4]
LncRNA CHRF negatively regulates miR-489 expression in CRC. [score:4]
CHRF knockdown increased the expression of miR-489 in HCT116 cells (P < 0.05, Figure 8D). [score:4]
Here, CHRF was overexpressed in CRC tissues compared to matched noncancerous tissues, and was inversely correlated miR-489 expression in CRC tissues. [score:4]
These results disclose that miR-489 inhibits the metastasis of CRC via regulating cell migration and invasion. [score:4]
miR-489 that was inversely regulated by long noncoding RNA cardiac hypertrophy-related factor (lncRNA CHRF) exerted an anti-metastatic role probably by targeting TWIST1/EMT signaling pathway. [score:4]
We next investigate whether miR-489 inhibits migration and invasion as well as EMT process of CRC cells by targeting TWIST1. [score:3]
miR-489 low -expressing CRC tissue showed strong staining of TWIST1 and Vimentin (A and E), and weak staining of E-cadherin (C). [score:3]
Thus, miR-489 suppresses EMT progression in CRC cells. [score:3]
In the present study, the expressions of miR-489 in the CRC tissues were prominently lower than those in the matched tumor-adjacent tissues. [score:3]
Spearman's correlation analysis revealed that the levels of miR-489 were inversely correlated with TWIST1 mRNA expression in CRC tissues (r = −0.43, P < 0.01, Figure 5E). [score:3]
In addition, the migratory and invasive abilities of HCT116 cells that were reduced by miR-489 overexpression were sequentially rescued by TWIST1 restoration (P < 0.05, Figure 7B and 7C). [score:3]
We revealed that miR-489 suppressed migration and invasion as well as EMT process of CRC cells. [score:3]
Taken together, our results verify that miR-489 may be served as a potential target for cancer therapeutics in CRC. [score:3]
Furthermore, our data suggest that underexpression of miR-489 was positively associated with advanced pT stage and pN stage as well as AJCC stage. [score:3]
While, weak signal of TWIST1 and Vimentin (B and F), and strong signal of E-cadherin (D) were observed in miR-489 high -expressing tumor. [score:3]
miR-489 overexpressing HCT116 cells showed the morphology of epithelial-like cells. [score:3]
In addition, miR-489 overexpression reduced the levels of TWIST1 mRNA and protein in HCT116 and HT29 cells (Figure 5C and 5D). [score:3]
Underexpression of miR-489 is observed in chemotherapy resistant breast cancer cells [16, 26, 27]. [score:3]
Notably, in vivo experiments revealed that miR-489 overexpression reduced the number of metastatic nodules in nude mice liver (P < 0.05, Figure 3). [score:3]
miR-489 has been found to be underexpressed in breast cancer [16], hypopharyngeal squamous cell carcinoma [17], ovarian cancer [18], lung cancer [19] and hepatocellular carcinoma (HCC) [20]. [score:3]
Spearman correlation analysis revealed that the levels of CHRF were inversely correlated with miR-489 expression in CRC tissues (r = −0.54, P < 0.01, Figure 8B). [score:3]
Reduced expression of miR-489 is confirmed in CRC. [score:3]
We demonstrated that miR-489 restoration inhibited migration and invasion as well as EMT of HCT116 cells, while miR-489 loss facilitated theses cellular behaviors of SW490 cells in vitro. [score:3]
While, weak signal of TWIST1 and Vimentin (Figure 6B and 6F), and strong signal of E-cadherin (Figure 6D) were observed in miR-489 high -expressing tumor. [score:3]
In conclusion, this work supported the first evidence that miR-489 was a potential prognostic biomarker and therapeutic target for CRC. [score:3]
Next, representative immunostaining showed that miR-489 low -expressing CRC tissue showed strong staining of TWIST1 and Vimentin (Figure 6A and 6E), and weak staining of E-cadherin (Figure 6C). [score:3]
Moreover, CHRF overexpression led to a notable reduction of miR-489 in SW480 cells (P < 0.05, Figure 8E and 8F). [score:3]
U6 and GAPDH were employed as reference genes to normalized the expression of miR-489, CHRF and TWIST1 mRNA, respectively. [score:3]
Figure 2(A) HCT116 cells that were transfected with precursor miR-489 and scrambled control, respectively, were subjected to qRT-PCR for miR-489 expression. [score:3]
Eighty CRC tissues and matched tumor-adjacent tissues were detected by qRT-PCR for miR-489 expression. [score:3]
In addition, an inverse correlation between miR-489 and TWIST1 mRNA expression was observed in CRC tissues. [score:3]
Moreover, lncRNA CHRF induced miR-489 loss facilitates migration and invasion as well as EMT probably via targeting TWIST1 in CRC cells. [score:3]
The expression and prognostic significance of miR-489 in CRC. [score:3]
s demonstrated that miR-489 overexpression notably reduced the luciferase activity of wt 3′-UTR of TWIST1 (P < 0.05, Figure 5B). [score:3]
Herein, luciferase activity assays indicated that TWIST1 was a direct downstream target of miR-489 in CRC. [score:3]
HE staining revealed that miR-489 overexpression significantly reduced liver metastases of HCT116 cells. [score:3]
Taken together, the CHRF-miR-489-TWIST/EMT signaling axis probably exerts key functions in the metastasis of CRC and may represent a therapeutic target for CRC patients. [score:3]
Figure 1(A) miR-489 expression differences between CRC tissues and matched tumor-adjacent tissues. [score:3]
This study showed that underexpression of miR-489 was correlated with poor prognostic features and reduced survival of CRC patients. [score:3]
The correlation between clinicopathological features and miR-489 expression in colorectal cancer. [score:3]
Clinical association analysis indicated that the low expression of miR-489 was positively associated with advanced pT stage and pN stage as well as AJCC stage (P < 0.05, respectively, Table 1). [score:3]
Thus, miR-489 is found to be inhibited during the carcinogenesis of CRC. [score:3]
In vivo experiments indicate that miR-489 overexpression prohibits initiation and growth of breast cancer in mice [29]. [score:3]
The expression status and role of miR-489 in human cancers is a controversial topic. [score:3]
As clinical association analysis showed that miR-489 underexpression was positively correlated with more aggressive phenotype of CRC, we speculated that miR-489 might modulate cancer cell migration and invasion. [score:3]
Firstly, our results demonstrate that miR-489 expression was reduced in CRC tissues and cell lines. [score:3]
Previous studies have reported that miR-489 is regulated by lncRNA CHRF [24, 25]. [score:2]
Modulating miR-489 expression had no effect on proliferation of CRC cells, as determined by MTT assays (Supplementary Figure 1). [score:2]
Thus, lncRNA CHRF contributes to TWIST1/EMT signaling pathway in CRC cells possibly by negatively regulating miR-489. [score:2]
miR-489 regulates migration and invasion of CRC cells. [score:2]
Accordingly, further studies were performed to confirm whether miR-489 regulated EMT process of CRC cells. [score:2]
Mutant (mt) 3′-UTR of TWIST1 was constructed by performing mutation on the binding sequences of miR-489. [score:2]
Further experiments revealed that miR-489 knockdown contributed to migration and invasion of SW480 cells (P < 0.05, respectively, Figure 2E and 2F). [score:2]
miR-489 is negatively regulated by lncRNA CHRF in CRC cells. [score:2]
miR-489 regulates TWIST1 abundance in CRC cells. [score:2]
Notably, we found the miR-489 inversely regulated TWIST1 abundance in CRC cells. [score:2]
Next, miR-489 knockdown was confirmed by qRT-PCR in SW480 cells (P < 0.05, Figure 2D). [score:2]
These data reveal that miR-489 functions as an anti-metastatic factor by regulating migration and invasion as well as EMT in CRC cells. [score:2]
miR-489 restrains EMT events in CRC cells. [score:1]
In conclusion, we show that miR-489 acts as an anti-metastatic factor in CRC. [score:1]
These results suggest that miR-489 may act as a promising prognostic marker for CRC patients. [score:1]
Figure 3HCT116 cells that were transfected with precursor miR-489 or scrambled control were injected to the spleen subcapsular. [score:1]
miR-489 restoration were performed in HCT116 cells after precursor miR-489 tranfection (P < 0.05, Figure 2A). [score:1]
miR-489 restrains EMT process of CRC cells. [score:1]
Then, we disclosed the biological function of miR-489 in CRC. [score:1]
Figure 4(A) HCT116 cells were transfected with precursor miR-489 and scrambled control, respectively. [score:1]
To verify this hypothesis, HCT116 and SW480, which showed the lowest and highest levels of miR-489, respectively, were used for gain- and loss-of-function experiments. [score:1]
Clinical significance of miR-489 in CRC patients. [score:1]
Then, our clinical data suggest that miR-489 may be used as a novel prognostic marker for CRC patients. [score:1]
But miR-489 restoration did not affected the luciferase activity of mt 3′-UTR of TWIST1 (Figure 5B). [score:1]
miR-489 loss promotes invasion and epithelial-mesenchymal transition (EMT) events of lung cancer cells [30]. [score:1]
Additionally, we supported the first evidence that underexpresion of miR-489 conferred a obvious poor prognosis of CRC patients. [score:1]
Quantitative data indicated that the levels of miR-489 in CRC tissues were significantly lower than those in matched noncancerous tissues (P < 0.05, Figure 1A). [score:1]
HCT116 cells that were transfected with precursor miR-489 or scrambled control were injected to the spleen subcapsular. [score:1]
In addition, miR-489 restoration restrains breast cancer cell proliferation, migration and invasion in vitro [28]. [score:1]
TWIST1 was considered as one of the candidates with which miR-489 could bind directly (Figure 5A). [score:1]
Moreover, TWIST1 restoration abrogated the effects of miR-489 on the migration, invasion and EMT process of CRC cells. [score:1]
TWIST1 restoration abolishes the effects of miR-489 in CRC cells. [score:1]
Figure 5(A) The potential miR-489 binding site in wild type (wt) 3′-UTR sequence of TWIST1. [score:1]
LncRNA CHRF induced miR-489 loss promotes EMT process of CRC cells. [score:1]
miR-489 loss facilitated EMT process and represented the morphology of mesenchymal-like cells. [score:1]
Thus, miR-489 potentially functions as a prognostic marker in CRC. [score:1]
[1 to 20 of 105 sentences]
3
[+] score: 118
We discovered that miR-148b, -27a and -489 are essential for the regulation of osteogenesis: miR-27a and miR-489 down-regulate while miR-148b up-regulates differentiation. [score:8]
0005605.g004 Figure 4(A–G) Transfection with inhibitors of miR-489 and -27a results in up-regulation of GCA protein expression. [score:8]
UNTR/Diff - untransfected differentiated cells, UNTR/Prop - untransfected undifferentiated cells, IC1,- cells transfected with Inhibitor Control Molecule 1, MC1,- cells transfected with Mimic Control Molecule 1, i27a - cells transfected with Inhibitor for miR27a, i489 - cells transfected with Inhibitor for miR489, m148b - cells transfected with mimic for miR148b. [score:7]
All together, these findings demonstrate that these three miRNA are both necessary and sufficient to modulate early osteogenesis in hMSC: miR-489 and miR-27a down-regulate and miR-148b up-regulates differentiation. [score:7]
However, inhibition of miR-27a demonstrated more substantial activation of SPP1 expression in comparison with inhibition of miR-489. [score:7]
Both miR-489 and -27a down-regulated osteogenesis, suggesting the possibility of common gene targets (Fig. 1b, 2b, Fig. S2). [score:6]
We hypothesize that if PEX7 is a key target of miR-27a and miR-489 then its knockdown may mimic effect of these miRNAs and inhibit osteogenic differentiation. [score:6]
Seven inhibitors were subsequently confirmed in independent experiments (Fig. 1b); six inhibitors (miR-489,-189,-153,-27a,-133a,-and -486) increased AP activity and one (hsa-miR-148b) decreased activity in differentiated hMSC. [score:5]
Interestingly, inhibition of miR-489 had a stronger effect on AP activity induction than inhibition of miR-27a. [score:5]
Analysis of the predicted gene targets revealed that APL, a gene encoding liver/bone/kidney-specific alkaline phosphatase, may be a target for miR-27a but not for miR-489. [score:5]
Inhibitor of miR-489 was able to stimulate differentiation in either propagation or differentiation conditions while inhibitor of miR-27a was active in the differentiation conditions only. [score:5]
RT-PCR -based study of gene expression demonstrated that both CHRD and PEX7 mRNA are present in hMSC but only PEX7 is regulated by miR-489 and -27a (Fig. S6a). [score:4]
In contrast, miR-489 was found to be down-regulated under similar conditions [23]. [score:4]
In a contrary, both RT-PCR -based study and immunohistochemistry -based analysis of gene expression demonstrated that GCA mRNA is present in hMSC and regulated by miR-489 and -27a (Fig. 4). [score:4]
Negative effect of miRNAs, miR-489 and -27a, on osteogenesis in hMSC is, at least in part, mediated by repression of GCA gene expression. [score:3]
Cells transfected with miR-489 inhibitor or miR-148b mimic alone or in combination demonstrated a drastic increase in total AP activity and in the number of AP -positive cells (Fig. 2a, Fig. S3). [score:3]
While further studies are needed to investigate the possible roles of miR-27a and -489 targets in greater detail, our data suggests that the inhibitory effect of miR-489 and -27a is, at least in part, mediated by repression of GCA. [score:3]
Expression of miR-489 was detected at very low levels in hMSC. [score:3]
Thus, while PEX7 still can be a target of miR-27a and miR-489 it may not mediate effect of these miRNAs on osteogeneis. [score:3]
miR-489 and -27a have 80 predicted targets in common (Table S3). [score:3]
Expression of miR-489 was detected at a very low level in undifferentiated MS cells and appeared to decrease even further upon differentiation. [score:3]
Surprisingly, transfection with miR-148b mimic, miR-489 or -27a inhibitors were able to rescue osteogenic potential in hMSC with high passage number. [score:3]
After induction of differentiation, expression of miR-489 becomes almost undetectable, decreasing 10-fold (p-value<0.1) (Table S1). [score:3]
Similarly, SPP1 may be a target for miR-489 but not for miR-27a. [score:3]
Additionally, we found that GCA 3′UTR reporter activity is regulated by miR-489 and -27a (Fig. S7). [score:2]
Figure S7GCA and PEX7 3′UTR reporter activity is regulated by miR-489 and -27a. [score:2]
In human cells, the miR-489 family is represented by a single member, miR-489. [score:1]
Figure S6 Effect of on osteogenesis miR-489 and -27a is not mediated by repression of CHRD or PEX7. [score:1]
The candidate miRNAs, miR-489, -27a and -148b, are representatives of three miRNA families. [score:1]
[1 to 20 of 29 sentences]
4
[+] score: 58
Other miRNAs from this paper: hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-148b, hsa-mir-133b
Although additional work will need to be done to clearly define the direct targets of miR-148b and miR-489, these miRNAs have been shown to be differentially regulated in osteoblasts exposed to specific graft materials (Palmieri et al., 2007, 2008), and their ability to affect osteogenesis in MSCs appears to be clear. [score:5]
In this study, hMSCs transfected with either a mimic of miRNA-148b (M-miR148b) or an inhibitor of miRNA-489 (I-miR489) increased ALP activity after 6 days when compared with cells that received non -targeting miRNA controls. [score:4]
To do this, hMSCs were transfected with a combination of both a mimic of miR-148b (M-miR148b) and an inhibitor of miR-489 (I-miR489) and allowed to differentiate in either CON medium or medium supplemented with soluble osteogenic factors (OST) in 2D culture plates. [score:3]
In the work presented here, we demonstrate that the transfection of hMSCs with a miR-148b mimic and a miR-489 inhibitor acts to sensitize these cells to exogenous osteogenic signals and greatly enhances the induction of bone-related tissue markers in both two-dimensional (2D) and engineered three-dimensional (3D) environments. [score:3]
The amount of collagen deposition in OST -treated hMSCs was increased in hMSCs transfected with M-miR148b + I-miR489 (Figure 1C), suggesting that these miRNAs accelerated collagen expression of osteogenic hMSCs. [score:3]
As shown in Figure 1C, collagen expression was also affected by of hMSCs with M-miR148b and I-miR489. [score:3]
In the work presented here, we demonstrate that the use of a miR-148b mimic and an miR-489 inhibitor has the effect of sensitizing hMSCs to soluble osteogenic factors, resulting in the rapid and robust induction of bone-related markers. [score:3]
2D studies were employed to quickly gain an understanding of the effects of M-miR148b and I-miR489 on osteogenic markers in hMSC cultures (Figures 1– 5) and direct the development of biomaterials for miRNA -based strategies. [score:3]
In order to confirm that the miRNA reagents effectively alter the expression levels of miR-148b and miR-489, sample plates were harvested after 48 h and analysed by qRT–PCR. [score:3]
hMSCs transfected with M-miR148b and I-miR489 showed significant increases in collagen 1A (COL1A) expression, independent of soluble osteogenic factors (OST medium; Figure 6D). [score:3]
Given that a combination of miRNA mimics and inhibitors were used for this experiment, we were interested in knowing whether the miRNAs were contributing equally to this robust induction of ALP activity or whether one of the miRNA reagents, either M-miR148b or I-miR489, was having a dominant effect on the cells. [score:3]
When statistically significant, the synergistic interaction between miRNA transfection (M-miR148b + I-miR489) and OST medium treatment is marked by symbols representing the p value for this interaction: [##] p < 0.05; * p < 0.01; ** p < 0.001 Figure 2 Individual components of OST medium were tested for their ability to induce (A) ALP activity, (B) calcium deposition and (C) collagen expression in 2D hMSC cultures. [score:3]
When statistically significant, the synergistic interaction between miRNA transfection (M-miR148b + I-miR489) and OST medium treatment is marked by symbols representing the p value for this interaction: [##] p < 0.05; * p < 0.01; ** p < 0.001 Figure 2 Individual components of OST medium were tested for their ability to induce (A) ALP activity, (B) calcium deposition and (C) collagen expression in 2D hMSC cultures. [score:3]
Error bars represent 95% CI Figure 6Transfection of hMSCs with M-miR148b (M-148b) and I-miR489 (I-489) enhances the osteogenic response to OST medium in 3D tissue constructs. [score:1]
Figure 1M-miR148b (M-148b) and I-miR489 (I-489) enhance the osteogenic activity of hMSCs. [score:1]
Also, when statistically significant, the synergistic interaction between miRNA transfection (M-miR148b + I-miR489) and OST medium treatment is marked by white symbols within the doubly-effected bars to identify the p value for this interaction: [##] p < 0.05; * p < 0.01; ** p < 0.001. [score:1]
These data indicate that M-miR148b, not I-miR489, plays a critical role in increasing collagen deposition in response to osteogenic media. [score:1]
As shown in Figure 1, the combination of M-miR148b and I-miR489 transfection and OST medium treatment appeared to have a synergistic effect on multiple markers of osteogenic differentiation (ALP activity, calcium deposition, and collagen accumulation). [score:1]
Given that the transfection of hMSCs with M-miR148b and I-miR489 appeared to predispose the cells to osteogenic signals, resulting in a more robust induction of osteogenic markers in response to the additional soluble factors present in OST medium, we wanted to identify the individual contributions of each of these media supplements on standard bone-related markers. [score:1]
These data suggest that M-miR148b and I-miR489 sensitized the hMSCs to the ostoegenic signals found in OST medium, resulting in quicker and/or more robust response to osteoinductive soluble factors. [score:1]
Transfected hMSCs showed a > 100-fold increase in miR-148b levels, while miR-489 levels were undetectable (data not shown), suggesting that the transfection process effectively alters miRNA levels in these cells. [score:1]
Error bars represent 95% CI Figure 6Transfection of hMSCs with M-miR148b (M-148b) and I-miR489 (I-489) enhances the osteogenic response to OST medium in 3D tissue constructs. [score:1]
When statistically significant, the synergistic interaction between miRNA transfection (M-miR148b + I-miR489) and OST medium treatment is marked by symbols representing the p value for this interaction: ## p < 0.05; * p < 0.01; ** p < 0.001. [score:1]
To test this, hMSCs were transfected with either M-miR148b or I-miR489 and cultured in OST medium for 20 days. [score:1]
As shown in Figure 3A, hMSCs transfected with M-miR148b showed elevated ALP activity over controls at day 5, whereas hMSCs transfected with I-miR489 showed little difference in ALP activity over the course of the study. [score:1]
Unlike its effect on ALP activity, in which the transfection of M-miR148b alone did not match cells transfected with both M-miR148b and I-miR489, M-miR148b transfection showed rates of calcium deposition similar to those of doubly -transfected cells. [score:1]
These data suggest that I-miR489 may work synergistically with M-miR148b, further enhancing its effect on ALP activity. [score:1]
The initial rate of calcium deposition in OST -treated hMSCs was increased in hMSCs transfected with M-miR148b + I-miR489 (Figure 1B), suggesting that these miRNAs accelerate bone-related mineralization of the extracellular environment. [score:1]
I-miR489 transfection appeared to have no effect on calcium deposition. [score:1]
[1 to 20 of 29 sentences]
5
[+] score: 46
Up-regulated expression of miR-572 (ΔΔCt = 2.161, p = 4.58E-06) and miR-663a (ΔΔCt = 1.911, p = 9.75E-06) were confirmed in fluoxetine -treated SK-N-SH cells, while the up-regulated expression of miR-489 (ΔΔCt = 1.2, p = 0.007), miR-572 (ΔΔCt = 3.392, p = 3.81E-07) and miR-663a (ΔΔCt = 1.94, p = 1.77E-06) were confirmed in fluoxetine -treated SH-SY5Y cells (Fig 3). [score:11]
Among the 13 miRNAs screened except miR-433, which was omitted from further analysis since the amplification was not proper in the cell lines studied, three miRNAs [miR-489 (p = 0.01 at 1μM), miR-572 (p = 0.009 at 1μM; p = 0.0004 at 5μM; p = 0.024 at 10μM); miR-663a (p = 0.032 at 5μM; p = 0.058 at 10μM)] were up-regulated in fluoxetine -treated (1-, 5- and 10-μM) SK-N-SH cells, while four miRNAs [miR-320a (p = 0.004 at 10μM), miR-489 (p = 0.037 at 10μM), miR-572 (p = 0.0002 at 5μM; p = 0.0004 at 10μM); miR-663a (p = 0.006 at 10μM)] were up-regulated in fluoxetine -treated SH-SY5Y cells compared to corresponding DMSO -treated control cells (Fig 2). [score:6]
In addition to miR-572 and miR-663a, the expression of miR-489 was up-regulated in fluoxetine -treated SH-SY5Y cells. [score:6]
Up-regulated expression of miRNAs (miR-320a, miR-489, miR-572 and miR-663a) in (a) SK-N-SH cells and (b) SH-SY5Y cells treated with various concentrations of fluoxetine compared to DMSO -treated control cells. [score:5]
miR-489, miR-572 and miR-663a were consistently up-regulated in fluoxetine -treated SK-N-SH and SH-SY5Y cells. [score:4]
The importance of miR-489 in synaptic transmission has been demonstrated in a mouse mo del of Alzheimer's disease [45]. [score:3]
Alteration of miR-489 and its target genes have been observed in postmortem brain samples from schizophrenic [43] and depressed suicidal patients [44]. [score:3]
In our previous study, target genes of miR-489 have been identified and predicted to be involved in important signalling systems such as MAPK, ErbB, TGF-beta and hedgehog signalling [24]. [score:3]
The expression of miR-320, miR-489, miR-572 and miR-663a were further compared between 10 μM fluoxetine (6 wells each) treated SK-N-SH and SH-SY5Y cells and their control cells. [score:2]
Confirmation qPCR experimental data with four miRNAs (miR-320, miR-489, miR-572 and miR-663a) of SH-SY5Y cells with 10-μM Fluoxetine and equal concentration of DMSO control. [score:1]
miR-489, a brain specific-miRNA [41, 42], has been implicated in the pathophysiology of various neuropsychiatric disorders [43– 46, 24]. [score:1]
Confirmation qPCR experimental data with four miRNAs (miR-320, miR-489, miR-572 and miR-663a) of SK-N-SH cells with 10-μM Fluoxetine and equal concentration of DMSO control. [score:1]
[1 to 20 of 12 sentences]
6
[+] score: 34
miR-151a-3p (ΔΔCt = -2.01, P = 8.29E-06), MiR-181b-5p (ΔΔCt = -3.39, P = 1.04E-10), miR-320a (ΔΔCt = -2.47, P = 5.02E-12), miR-328 (ΔΔCt = -2.28, P = 4.33E-06), miR-433 (ΔΔCt = -2.33, P = 0.0001), miR-489 (ΔΔCt = -2.10, P = 1.25E-06), miR-572 (ΔΔCt = -2.47, P = 2.66E-08) and miR-663a (ΔΔCt = -2.06, P = 0.00002) were downregulated, while miR-101-3p (ΔΔCt = 1.43, P = 0.003), miR-106b-5p (ΔΔCt = 1.30, P = 0.008), miR-130a-3p (ΔΔCt = 2.35, P = 1.89E-09), miR-195-5p (ΔΔCt = 1.43, P = 0.0016) and miR-19b-3p (ΔΔCt = 1.87, P = 6.88E-09) were upregulated in the ASD individuals. [score:7]
MiR-151a-3p, miR-181b-5p, miR-320a, miR-328, miR-433, miR-489, miR-572, and miR-663a were downregulated, while miR-101-3p, miR-106b-5p, miR-130a-3p, miR-195-5p, and miR-19b-3p were upregulated. [score:7]
miR-151a-3p, miR-181b-5p, miR-320a, miR-328, miR-433, miR-489, miR-572 and miR-663a were downregulated while miR-101-3p, miR-106b-5p, miR-19b-3p, miR-195-5p, miR-130a-3p and miR-27a-3p were upregulated. [score:7]
MiR-151a-3p, miR-181b-5p, miR-320a, miR-328, miR-433, miR-489, miR-572 and miR-663a were downregulated, while miR-101-3p, miR-106b-5p, miR-19b-3p, miR-195-5p, miR-130a-3p and miR-27a-3p were upregulated. [score:7]
The differentially expressed miRNAs in this study, which included miR-101, miR-106b, miR-130a, miR-151a, miR181b, miR-328, miR-433, miR-489 and miR-572, were previously reported to have altered expression in schizophrenia [31- 35], supporting the contention that ASD and schizophrenia share common neurobiological features [36]. [score:5]
The Ct values of nine miRNAs (miR-101-3p, miR-106b-5p, miR-151a-3p, miR-195-5p, miR-19b-3p, miR-27a-3p, miR-320a, miR-328, and miR-489) were in the range of 25–30, while the remaining five miRNAs (miR-130a-3p, miR-181b-5p, miR-433, miR-572, and miR-663a) had Ct values in the range of 30 to 35. [score:1]
[1 to 20 of 6 sentences]
7
[+] score: 30
These authors observed that miR-489 was underexpressed in this type of cancer, especially through the MAPK pathway, In a later in vitro experiment in xenograft mice, they determined that overexpression of this microRNA in HER2 -positive breast cancer cells significantly inhibited cell growth and decreased tumorigenicity and tumor growth. [score:7]
Further validation of the top ranked microRNAs revealed significant differences in the expression of 6 of them in relation to UA, 7 in relation to SA and 1 (miR-489) that was related to both types. [score:3]
In our study, we were able to recognize significant differences in miR-489 expression between SA and UA. [score:3]
Based on these facts, it could be suggested that the differences found in miR-489 expression between the two types of ameloblastoma could play an important role to explain the different aggressiveness observed in these entities. [score:3]
The differences in miR-489 expression could be an important element in the differential diagnosis between the two types of ameloblastomas, and therefore, it is essential to confirm these results in a larger set of samples. [score:3]
Although the information on the functions of miR-489 so far is scarce, Schoolmeesters et al. [43] pointed out that this microRNA could regulate the early osteogenic differentiation in human mesenchymal stem cells, and play a critical role in the osteogenic process. [score:2]
After applying the inclusion criteria (|FC| <0.2 or> 5 and p adjusted <0.05), as previously mentioned, biological validation was performed by RT-qPCR of the 13 differently regulated miRNAs (hsa-miR-9, hsa-miR-135b*, hsa-miR-194*, hsa-miR-489, hsa-miR-592, hsa-miR-369-5p, hsa-miR-876-5p, hsa-miR-31, hsa-miR-135b, hsa-miR-211, hsa-miR-944, hsa-miR-142-5p, hsa-miR-455-3p), in an independent set of 46 samples corresponding to 19 SA, 8 UA and 19 controls. [score:2]
In summary, these authors suggest that these results define a double -negative feedback loop involving miR-489 and the HER2-SHP2-MAPK signaling axis that can regulate breast cancer cell proliferation and tumor progression and might have therapeutic relevance for HER2 -positive breast cancer [47]. [score:2]
After validation, we recognized significant differences in 6 microRNAs in relation to UA, 7 to SA and in 1 (miR-489) in relation to both tumor types. [score:1]
When comparing the SA group with the UA group, we only found statistically significant differences for microRNA-489 (p = 0.016) (Table 2). [score:1]
In addition, we identified a microRNA (miR-489) that is suggestive of differentiating among solid from unicystic ameloblastoma. [score:1]
We consider that these results demonstrate a specific profile of altered microRNAs for these neoplasms, and the existence of a microRNA (miR-489) that is suggestive of differentiating between the two major types of ameloblastoma. [score:1]
In addition, we identified a microRNA (miR-489) suggestive of differentiating between solid and unicystic ameloblastomas. [score:1]
[1 to 20 of 13 sentences]
8
[+] score: 24
We found that miR-15a-3p (0.1-fold) and miR-30a-5p (0.2-fold) were down-regulated and miR-489-3p up-regulated (2 fold) in ATLOs (Figure 3). [score:7]
The three miRNAs, miR-15a-3p, miR-30a-5p and miR-489-3p, were down-regulated 0.6-, 0.25- and 0.2-fold, respectively (Figure 3). [score:4]
Wang K. Liu F. Zhou L. Y. Long B. Yuan S. M. Wang Y. Liu C. Y. Sun T. Zhang X. J. Li P. F. The long noncoding RNA CHRF regulates cardiac hypertrophy by targeting miR-489 Circ. [score:4]
These latter data confirmed the interest to study individually the cells as shown by the inverse expression of miR-489-3p in the whole aneurysmal aorta. [score:3]
MiR-489-3p was identified in hypertrophic cardiomyocytes but its expression was reduced after angiotensin treatment [33]. [score:2]
Based on the average of their normalized values, we selected the top three miRNAs with a difference of value <1: miR-15a-3p, miR-30a-5p, miR-489-3p for further analysis by qRT-PCR. [score:1]
Despite limitations due to the small sample size in the array and PCR experiments, the miRNA profiling of isolated ATLOs enabled the detection of 164 miRNAs out of 850 miRNAs screened, and the three miRs with the highest expression (miR-15a-3p, miR-30a-5p and miR-489-3p) were further characterized. [score:1]
Figure 4Relative plasma quantification of the three miRNAs (mir-15a-3p (A); miR-30a-5p (B); miR-489-5p (C)) in patients with AAA (n = 20) and with PAD without AAA (n = 17) by qRT-PCR using the −2ΔΔ C [t] method, with PAD patients as reference and Syn-Cel-miR-39 for calibration. [score:1]
Concerning miR-489-3p, we found a similar modulation for M1 (28.8-fold) and M2 (5.4-fold) macrophages. [score:1]
[1 to 20 of 9 sentences]
9
[+] score: 22
However, we note that miR-489 expression in CC founders suggests three distinct groups (high expression group composed of NOD/ShiLtJ and WSB/EiJ; medium expression group composed of A/J, C57BL/6J, 129S1SvImJ, and NZO/H1LtJ; and low expression group composed of CAST/EiJ and PWK/PhJ), but the allele effects for the eQTL on chromosome (Chr) 6 indicates that this eQTL only explains the differences between CAST/EiJ and PWK/PhJ vs. [score:9]
Taken together, these results indicate that cis-regulatory elements at the respective eQTL are the primary determinants of miR-489 and miR-342-3p expression in the lung. [score:4]
Thus it appears that one or more additional loci likely contribute to miR-489 expression; but we did not identify other eQTL (local or distant) using genome scans in which we conditioned on the Chr 6 eQTL. [score:3]
Expression of miR-489 in CC founders (a) and preCC mice (b) as a function of founder haplotype at the eQTL on chromosome 6. CC founder miRNA expression was measured by microarray while preCC miRNA expression was measured by qRT-PCR and data for the latter are presented as −1*DeltaCq (normalized to miR-17*). [score:3]
We note in particular the bimodal distributions for two miRNAs, miR-133 and miR-489, suggesting a single, large-effect eQTL for each. [score:1]
Two eQTL, for miR-489 and miR-342-3p, stood out in terms of effect size. [score:1]
Fig. 3 A large effect local eQTL for miR-489. [score:1]
[1 to 20 of 7 sentences]
10
[+] score: 22
Other miRNAs from this paper: hsa-mir-148a, hsa-mir-152, hsa-mir-148b
We have previously shown that miRNA-489 could directly target and suppress SPIN1 expression in breast cancer [11]. [score:8]
Here we used miRNA-489 as a tool to downregulate SPIN1 expression in MCF-7/ADM cells. [score:6]
We have previously found that miR-489 could directly target SPIN1 in breast cancer [11]. [score:4]
Moreover, we have previously found that SPIN1 was directly regulated by microRNA-489 [11]. [score:3]
Lentiviruses miRNA-489 or miRNA control was stably transfected into cells. [score:1]
[1 to 20 of 5 sentences]
11
[+] score: 20
Here we found that 13 of the 349 miRNAs examined were aberrantly expressed in samples from the 2-mg/kg–treated animals, and two down-regulated miRNAs (rno-let-7e* and rno-miR-489) were consistent with the up- regulation of mRNA expression of their predicted target genes, Bcl10 and Ccna2. [score:11]
Using miRGen and MicroCosm, we found that Ccna2 and Bcl10, two genes that were up-regulated in our mRNA arrays, were the predicted targets of the down-regulated rno-miR-489 and rno-let-7e*, respectively. [score:9]
[1 to 20 of 2 sentences]
12
[+] score: 20
In the present study, we examined the levels of a group of miRNAs, which had been reported to regulate the expression of pluripotent genes such as miR-489, miR-370 and miR-433 30, or were predicted to target stem cell pluripotency genes such as miR-7 and miR-21. [score:6]
showed that miR-489, miR-370 and miR-433 were highly expressed in spheroid hMSCs compared to monolayer hMSCs, especially miR-370 with a fivefold increase, while let-7f, miR-7, miR-145, miR-21 and miR-24 were down-regulated in spheroid hMSCs (Fig. 5A). [score:5]
Our results showed that miR-489, miR-370 and miR-433 were highly expressed in spheroid hMSCs, while miR-7, miR-145, let-7f, miR-21 and miR-24 were down-regulated in spheroid hMSCs, compared to hMSCs that had been cultured in monolayer. [score:5]
To understand whether miRNAs were involved with the phenotypical changes of hMSCs in spheroids, real-time PCR analysis was performed to examine the expression of miR-489, miR-370, miR-433, let-7f, miR-7, miR-145, miR-21 and miR-24. [score:3]
MiR-489, miR-370 and miR-433 have recently been found to play an important role in maintaining the quiescent state of adult stem cells 30. [score:1]
[1 to 20 of 5 sentences]
13
[+] score: 17
We used the miRDB[91, 92] to identify novel miRNA targets (Additional file 2), and we found that the 9 different miRNAs that increased in CD30 [hi] lymphocytes target several genes associated with neoplastic processes (Additional file 2): gga-mir-204 targets FAS apoptosis inhibitory molecule 2, RAB22A (a RAS oncogene family member) and HDAC 9; gga-mir-489 targets FAS associated factor 1 (FAF1) and gga-mir-7 targets RAS related viral oncogene homolog 2. Except FAF1 (which was unchanged) none of these proteins were identified and so we cannot confirm the upregulated miRNA’s potential effects on neoplasia in CD30 [hi] cells. [score:16]
Of these, nine (gga-mir-1b, gga-mir-7, gga-mir-7b, gga-mir-10b, gga-mir-31, gga-mir-130b, gga-mir-204, gga-mir-215, gga-mir-489) are increased, and five (gga-mir-223, gga-mir-124b, gga-mir-140, gga-mir-183, gga-mir-222a) are decreased in CD30 [hi] cells. [score:1]
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14
[+] score: 17
Mir-489 is expressed in the adipocyte precursor mesenchymal stem cells, where its expression inhibits differentiation into osteoblasts [68]. [score:6]
Two of the additional differentially expressed miRNAs from the sequencing data, mir-34c and mir-489 could not be analyzed by qPCR due to very low expression in the majority of the samples. [score:5]
Also mir-489 and mir-34c could not be detected in all animals due to very low expression, and were therefore excluded from the qPCR analysis. [score:3]
Differential expression in the sequencing data from the lean and obese pigs was calculated using the DESeq2 package in R and revealed six significantly differentially expressed miRNAs between the two groups: mir-9-5p, mir-124a-3p, mir-9-3p, mir-199a-5p, mir-489-3p and mir-34c-3p. [score:3]
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15
[+] score: 16
Furthermore, they identified a lncRNA named cardiac hypertrophy related factor (CHRF) that acts as an endogenous sponge of miR-489 and thus downregulates its expression [63]. [score:6]
Wang K. Liu F. Zhou L. Y. Long B. Yuan S. M. Wang Y. Liu C. Y. Sun T. Zhang X. J. Li P. F. The long noncoding RNA CHRF regulates cardiac hypertrophy by targeting miR-489 Circ. [score:4]
Moreover, they showed that MYD88 is a direct target of miR-489 in cardiac hypertrophy. [score:4]
Wang et al. used microarray analyses to show that angiotensin II treatment reduced the levels of miR-489 in patients with cardiac hypertrophy (Table 2 and Figure 2). [score:1]
Therefore, one can anticipate a therapeutic regimen for maladaptive cardiac hypertrophy that works by modulating the levels of miR-489 and CHRF. [score:1]
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16
[+] score: 15
Expression of precursor and mature miRNA of differentially expressed cellular miRNAs (A) miR-489, -630 in HOK and (B) miR-23a, -33a, -155, -489, and 943 in Mφ were determined by RT-qPCR. [score:5]
In contrast, the expression of mature miR-489, but not pre-miR-489 levels were significantly induced in miR-K12-3-3p -transfected cells (Figure 4A; lower panel). [score:3]
To address this, expression of mature and pre-miRs of miR-489 and miR-630 (from HOK) and miR-23a, miR-33a, miR-155, miR-489, and miR-943 (from Mφ) was examined. [score:3]
For Mφ, we noted similar expression profiles of mature and precursor miRNA for miR-155, miR-943, and miR-489 (Figure 4B; upper and middle panel). [score:3]
Similar correlation in the mature and precursor miRNA was also observed for miR-630, miR-943, miR-489 (Mφ). [score:1]
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17
[+] score: 14
Under cardiomyopathy conditions, lncRNA CHRF is expressed and acts as a sponge for microRNA-489, preventing it from exerting its function, which is the downregulation of Myd88 (a known inducer if cardiac hypertrophy). [score:6]
The long noncoding RNA CHRF regulates cardiac hypertrophy by targeting miR-489. [score:4]
Under these conditions, microarray profiling experiments were able to identify microRNA-489 as a significantly downregulated transcript. [score:4]
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18
[+] score: 11
Decreasing gene SOX4, was identified as a potential target for miR-489 from group I. The identification of 19 microRNAs with decreasing expression along the pancreatic development, thus contributing to the upregulation of their potential targets, suggests a collaborative network of microRNAs and mRNAs during this period (Figure. [score:11]
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19
[+] score: 11
Down-regulation of miR-489 and subsequent activation of the RAS-MAPK pathway mediated by an enhanced SHP2 activity could represent a critical oncogenic event in HSCC. [score:4]
MiR-489 was one of the most down-regulated miRNAs in hypopharyngeal squamous cell carcinoma (HSCC). [score:4]
Kikkawa et al. identified PTPN11 mRNA as a bona fide target of miR-489 [43]. [score:3]
[1 to 20 of 3 sentences]
20
[+] score: 11
Also, miR-221 and miR-222 were upregulated while miR-21, miR-342, and miR-489 were downregulated in tamoxifen-resistant MCF-7 cells; the reintroduction of miR-221 or miR-222 rendered the parent MCF-7 cells resistance to tamoxifen through inhibiting their target p27Kip1, which was reduced by 50% in resistant cells [17]. [score:11]
[1 to 20 of 1 sentences]
21
[+] score: 10
Using our mo del, we discovered human encoded miRNAs hsa-miR-489, hsa-miR-325, hsa-miR-876-3p and hsa-miR-2117 targeting HA, PB2, MP and NS of influenza A, respectively. [score:3]
hsa-miR-489, hsa-miR-325, hsa-miR-876-3p and hsa-miR-2117 are predicted to target HA, PB2, MP and NS of influenza A, respectively. [score:3]
Our mo del identified some key miRNAs including hsa-miR-489, hsa-miR-325, hsa-miR-876-3p and hsa-miR-2117, which target HA, PB2, MP and NS of H1N1, respectively. [score:3]
The number of binding sites of hsa-miR-489 is the least, and only the seed region was paired. [score:1]
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22
[+] score: 10
Other miRNAs from this paper: hsa-mir-106a, hsa-mir-34a, hsa-mir-149, hsa-mir-200c, hsa-mir-375
Based on this, we found that miR-489 and its target Smad3 regulate chemoresistance via the EMT pathway 13, suggesting such analysis could simplify the way to find important miRNAs and its targets regulating chemoresistance, and again indicating the important role of the EMT in the regulation of chemoresistance. [score:8]
Among those, we have validated EMT transcriptional factor SMAD3 is regulated by miR-489 to develop chemoresistance in breast cancers 13. [score:2]
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23
[+] score: 9
Interestingly, miR-489 was found to be the most overexpressed miRNA between adenoma subtypes though its downregulation was observed in CRC and was also associated with other tumor types (Additional file 1: Table S1) [53, 54]. [score:6]
miR-489 expression showed the greatest difference between adenoma subtypes with a > 4.5-fold increase in tubulovillous adenoma samples. [score:3]
[1 to 20 of 2 sentences]
24
[+] score: 7
Wu, Q. et al. miR-489 inhibits silica -induced pulmonary fibrosis by targeting MyD88 and Smad3 and is negatively regulated by lncRNA CHRF. [score:6]
To confirm the therapeutic importance of miRNAs in silica -induced pulmonary fibrosis, our previous work have revealed that miR-486-5p and miR-489 play important anti-fibrotic roles in silica -induced pulmonary fibrosis 15, 16. miR-503, located on the chromosome Xq26.3, is an intragenic miRNA, and belongs to the miR-16 family [17]. [score:1]
[1 to 20 of 2 sentences]
25
[+] score: 6
MiR-324-5p (FC = 6.26, p = 0.003) and miR-489 (FC = 9.34, p = 0.006) exhibited the greatest degree of up-regulation in the presence of IFN-α while miR-30c and miR-130a demonstrated the greatest difference in expression between HCV-infected Huh7.5 cells treated with or without IFN-α (Fig. 3C). [score:6]
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26
[+] score: 4
Jiang and his colleagues proved that forced -expression of miR-489 reversed resistance to doxorubicin in doxorubicin resistant MCF-7/ADM cells by regulating epithelial-mesenchymal transition (EMT) properties [29]. [score:4]
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27
[+] score: 4
Other miRNAs from this paper: hsa-mir-218-1, hsa-mir-218-2
The long noncoding RNA CHRF regulates cardiac hypertrophy by targeting miR-489. [score:4]
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28
[+] score: 4
Additional precursor sequences of miRNAs containing in dels include miR-520h [39], [40], [41], miR-486 [42], miR-489 [43], miR-223 [44], miR-373 [45], miR-630 [46] and miR-1233 [17], which have been shown to be involved in cancer development, and miR-631, which is associated with risk of coronary artery disease [47]. [score:4]
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29
[+] score: 4
[32] A recently identified lncRNA, CHRF, was demonstrated to regulate cardiac hypertrophy by targeting miRNA-489 (Wang et al. [33]). [score:4]
[1 to 20 of 1 sentences]
30
[+] 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-17, hsa-mir-21, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-30a, hsa-mir-31, hsa-mir-96, hsa-mir-99a, hsa-mir-16-2, hsa-mir-30c-2, hsa-mir-30d, hsa-mir-182, hsa-mir-183, hsa-mir-211, hsa-mir-217, hsa-mir-218-1, hsa-mir-218-2, hsa-mir-221, hsa-mir-222, hsa-let-7g, hsa-let-7i, hsa-mir-15b, hsa-mir-23b, hsa-mir-30b, hsa-mir-125b-1, hsa-mir-132, hsa-mir-143, hsa-mir-145, hsa-mir-191, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-126, hsa-mir-184, hsa-mir-190a, hsa-mir-195, rno-mir-322-1, rno-let-7d, rno-mir-335, rno-mir-342, rno-mir-135b, hsa-mir-30c-1, hsa-mir-299, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-379, hsa-mir-382, hsa-mir-342, hsa-mir-135b, hsa-mir-335, rno-let-7a-1, rno-let-7a-2, rno-let-7b, rno-let-7c-1, rno-let-7c-2, rno-let-7e, rno-let-7f-1, rno-let-7f-2, rno-let-7i, rno-mir-15b, rno-mir-16, rno-mir-17-1, rno-mir-21, rno-mir-23a, rno-mir-23b, rno-mir-24-1, rno-mir-24-2, rno-mir-25, rno-mir-26a, rno-mir-26b, rno-mir-30c-1, rno-mir-30e, rno-mir-30b, rno-mir-30d, rno-mir-30a, rno-mir-30c-2, rno-mir-31a, rno-mir-96, rno-mir-99a, rno-mir-125a, rno-mir-125b-1, rno-mir-125b-2, rno-mir-126a, rno-mir-132, rno-mir-143, rno-mir-145, rno-mir-183, rno-mir-184, rno-mir-190a-1, rno-mir-191a, rno-mir-195, rno-mir-211, rno-mir-217, rno-mir-218a-2, rno-mir-218a-1, rno-mir-221, rno-mir-222, rno-mir-299a, hsa-mir-384, hsa-mir-20b, hsa-mir-409, hsa-mir-412, hsa-mir-494, rno-mir-489, rno-mir-412, rno-mir-543, rno-mir-542-1, rno-mir-379, rno-mir-494, rno-mir-382, rno-mir-409a, rno-mir-20b, hsa-mir-542, hsa-mir-770, hsa-mir-190b, hsa-mir-543, rno-mir-466c, rno-mir-17-2, rno-mir-182, rno-mir-190b, rno-mir-384, rno-mir-673, rno-mir-674, rno-mir-770, rno-mir-31b, rno-mir-191b, rno-mir-299b, rno-mir-218b, rno-mir-126b, rno-mir-409b, rno-let-7g, rno-mir-190a-2, rno-mir-322-2, rno-mir-542-2, rno-mir-542-3
Occasionally, expression of rno-miR-489 was most noticeable in the theca and cumulus cells of FC. [score:3]
These included rno-miR-24, rno-miR-31, rno-miR-96, rno-miR-183, rno-miR-222, rno-miR-489, U6 snRNA (positive control) and scrambled miRNA (negative control). [score:1]
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31
[+] score: 3
This functional node includes miR-489 and miR-99a, although no correlation was found between their expression and functional node activity. [score:3]
[1 to 20 of 1 sentences]
32
[+] score: 3
Next, to further explore the functions of these miRNAs in HCC, we selected miRNAs with a fold change >5, namely hsa-miR-636, hsa-miR-671, hsa-miR-489, hsa-miR-26a, hsa-miR-320, hsa-miR-628, hsa-miR-505, hsa-miR-100, hsa-miR-664, hsa-miR-942, hsa-miR-192, hsa-miR-99b, hsa-miR-125b, hsa-miR-10b, hsa-miR-30b, and hsa-miR-145, for GO (Gene Ontology) enrichment analysis [21] of their target genes using the web -based software WebGestalt 2.0 [22]. [score:3]
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33
[+] score: 3
In the first group, there were 19 miRNAs with an expression level that was four times higher in BCSCs than in MCF-7 cells: miR-122a, miR-152, miR-212, miR-224, miR-296, miR-31, miR-373*, miR-489, PRED_MIR127, PRED_MIR154, PRED_MIR157, PRED_MIR162, PRED_MIR165, PRED_MIR191, PRED_MIR207, PRED_MIR219, PRED_MIR246, PRED_MIR88 and PRED_MIR90. [score:3]
[1 to 20 of 1 sentences]
34
[+] score: 3
Authors performed array -based miRNA profiling in MDA-MB-231 breast cancer cell derivatives highly metastatic to bone and lung, and found a signature of six genes (miR-335, miR-126, miR-206, miR-122a, miR-199a*, and miR-489) whose expression was highly decreased in metastatic cells. [score:3]
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35
[+] score: 2
Furthermore, five of the identified novel miRNAs share considerable sequence homology with oncogenic miRNAs (oncomiRs) including miR-590 [29], miR-196 27, 28, miR-489 [26], miR-508 [30] and miR-143 [31]. [score:1]
Several identified novel miRNAs closely matched the sequences of annotated miRNAs of known physiological function that have been demonstrated to play a role in oncogenesis (Fig.   3), including miR-489 [26], miR-196 27, 28, miR-590 [29], miR-508 [30] and miR-143 [31]. [score:1]
[1 to 20 of 2 sentences]
36
[+] score: 2
Other miRNAs from this paper: hsa-let-7d, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-17, hsa-mir-21, hsa-mir-22, hsa-mir-30a, hsa-mir-32, hsa-mir-33a, hsa-mir-148a, hsa-mir-30c-2, hsa-mir-30d, hsa-mir-147a, hsa-mir-34a, hsa-mir-187, hsa-mir-204, hsa-mir-205, hsa-mir-200b, hsa-mir-23b, hsa-mir-30b, hsa-mir-125b-1, hsa-mir-138-2, hsa-mir-142, hsa-mir-144, hsa-mir-125b-2, hsa-mir-138-1, hsa-mir-146a, hsa-mir-190a, hsa-mir-200c, hsa-mir-155, hsa-mir-30c-1, hsa-mir-200a, hsa-mir-30e, hsa-mir-365b, hsa-mir-328, gga-mir-33-1, gga-mir-125b-2, gga-mir-155, gga-mir-17, gga-mir-148a, gga-mir-138-1, gga-mir-187, gga-mir-32, gga-mir-30d, gga-mir-30b, gga-mir-30a, gga-mir-30c-2, gga-mir-190a, gga-mir-204-2, gga-mir-138-2, gga-let-7d, gga-let-7f, gga-mir-146a, gga-mir-205b, gga-mir-200a, gga-mir-200b, gga-mir-34a, gga-mir-30e, gga-mir-30c-1, gga-mir-205a, gga-mir-204-1, gga-mir-23b, gga-mir-142, hsa-mir-449a, hsa-mir-146b, hsa-mir-548a-1, hsa-mir-548a-2, hsa-mir-548a-3, hsa-mir-33b, hsa-mir-449b, gga-mir-146b, gga-mir-147, gga-mir-489, gga-mir-449a, hsa-mir-449c, gga-mir-21, gga-mir-144, gga-mir-460a, hsa-mir-147b, hsa-mir-190b, gga-mir-22, gga-mir-460b, gga-mir-1662, gga-mir-1684a, gga-mir-449c, gga-mir-146c, gga-mir-449b, gga-mir-2954, hsa-mir-548aa-1, hsa-mir-548aa-2, 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-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, gga-mir-365b, gga-mir-33-2, gga-mir-125b-1, gga-mir-190b, gga-mir-449d, gga-mir-205c
We also identified five other microRNAs including miR-489-3p, miR-1662, miR-460b-5p, miR-144-3p and miR-30e-5p, which were involved in the regulation of HIF1α in these data. [score:2]
[1 to 20 of 1 sentences]
37
[+] score: 2
Recently, decreased miR-489 has been reported upon hyperoxia exposure in neonatal mice and humans with BPD [49]. [score:1]
The authors suggest that decreased miR-489 may be inadequate attempts at compensation [49]. [score:1]
[1 to 20 of 2 sentences]
38
[+] score: 1
Although circulation levels of miR-29b, miR-30a, miR-30d, miR-103, miR-126-5p, miR-144, miR-155, miR-425-5p, miR-489, miR-1249, and miR-2888 were also examined, no significant differences in these miRNAs were observed between the cattle groups at any time points or between the time points in either of the cattle groups. [score:1]
[1 to 20 of 1 sentences]
39
[+] score: 1
Recent studies have documented that selected miRNAs, such as miR-451, miR-487a, miR-489, and miR-125b play key roles in the chemoresistance of breast cancer [5]. [score:1]
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40
[+] score: 1
Notably, six miRNAs (miR-489, miR-194–3p, miR-200a-3p, miR-30e-3p, miR-192, and miR-574–3p) were identically decreased in both our microarrays and The Cancer Genome Atlas (TCGA) dataset (Supplementary Table 1, Figure 1B). [score:1]
[1 to 20 of 1 sentences]
41
[+] score: 1
The 12 miRNAs (miR-23b, miR-25, miR-27b, miR-93, miR-106b, miR-189, miR-489, miR-505, miR-542-5p, miR-565, miR-652, and let-7d) were transfected into MCF7-ADR-Luc cells (Figure 4F). [score:1]
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42
[+] score: 1
Other miRNAs from this paper: hsa-mir-32, hsa-mir-653, bta-mir-32, bta-mir-653, bta-mir-489
In the second region, all three genes were identified: CALCR, MIR653, and MIR489. [score:1]
[1 to 20 of 1 sentences]
43
[+] score: 1
66 hsa-miR-511 −4.05 16.61 hsa-miR-26b −4.01 16.15 hsa-miR-210 −4.01 16.15 hsa-miR-489 −3.98 15.78 hsa-miR-22* −3.98 15.74 hsa-miR-15a* −3.97 15.70 hsa-miR-106a −3.92 15.15 hsa-miR-331-5p −3.91 15.04 hsa-miR-194 −3.88 14.73 hsa-miR-139-5p −3.85 14.38 hsa-miR-193a-5p −3.84 14.37 hsa-miR-29a −3.80 13.94 hsa-miR-24 −3.75 13.43 hsa-miR-140-5p −3.71 13.12 hsa-miR-28-3p −3.69 12.91 hsa-miR-151-3p −3.67 12. [score:1]
[1 to 20 of 1 sentences]
44
[+] score: 1
Other miRNAs from this paper: hsa-mir-31, hsa-mir-216a, hsa-mir-217
For instance, miR-489 modulated chemoresistance through EMT-related pathway in breast cancer [27]. [score:1]
[1 to 20 of 1 sentences]
45
[+] score: 1
Other miRNAs from this paper: mmu-mir-489
Since miR-489 has been previously shown to be important for the breakage of satellite cell quiescence [34], it would be interesting to study whether FGF6 and FGF19 induce miR-489 or synergize with its effects. [score:1]
[1 to 20 of 1 sentences]
46
[+] score: 1
The PCA analysis identified a representative miRNA (miR-548c-3p, miR-139-3p, miR-489, and miR-454*) for each of the four clusters. [score:1]
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