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28 publications mentioning rno-mir-31b

Open access articles that are associated with the species Rattus norvegicus and mention the gene name mir-31b. 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: 493
DEN -induced rat HCC tissues showed the upregulated expression levels of HDAC2, CDK2, cyclin D1, cyclin A, N-cadherin, fibronectin and suppressed expression levels of p21 [WAF1/Cip1] and E-cadherin accompanied by reduced-miR31 expression compared to normal rat hepatic tissues (Fig. 5B and C). [score:11]
Our results showed inhibition of DNA methylation by either 5-aza-dC treatment or knockdown of DNMT1 caused the induction of miR-31 expression, and consequently suppressed HDAC2 and CDK2 expression in liver cancer cells. [score:10]
Therefore, we hypothesized that some cancer-driver genes targeted by miR-31 are up-regulated in HCC as miR-31 was down-regulated in HCC. [score:9]
MiR-31 was significantly down-regulated in overt HCC and ectopic expression of miR-31 mimics inhibited in vitro tumor growth and metastatic ability in liver cancer cell lines. [score:8]
In this study, we showed that miR-31 expression was significantly down-regulated in a subset of HCCs, and the low expression of miR-31 was associated with a poor prognosis in HCC patients. [score:8]
As a tumor suppressive role of miR-31 in tumorigenesis, it was reported that miR-31 directly or indirectly controls expressions of specific proteins involving hallmarks of cancers, such as cell cycle, apoptosis, migration and cytoskeleton regulating molecules. [score:8]
The fact that HDAC2 and CDK2 are up-regulated in HCC led us to hypothesize that normal HDAC2 and CDK2 expressions are balanced by endogenous miR-31, which selectively controls HDAC2 and CDK2 mRNA translation in normal hepatic liver cells. [score:8]
Disruption of DNA methylation by either 5-aza-dC treatment or DNMT1 knockdown caused the induction of miR-31 expression, and thereby suppressed HDAC2 and CDK2 expression in both SNU-449 and SKHep-1cells (Fig. 6D and E). [score:8]
In our study, western blot analysis showed that HDAC2 and CDK2 protein levels were decreased after ectopic expression of miR-31, and simultaneously induced p21 [WAF1/Cip1] and suppressed the expression of cyclin A and cyclin D in both SNU-449 and SKHep-1 cells. [score:7]
For liver cancer, one recent study reported that miR-21, miR-31, miR-122, miR-221, miR-222 were significantly up-regulated in HCC tissues, whereas miR-145, miR-146a, miR-200c, and miR-223 were found to be down-regulated [15]. [score:7]
Furthermore, in prostate cancer, miR-31 was identified to negatively regulate E2F1, E2F2, EXO1, FOXM1, and MCM2, which are the key regulatory proteins in cell cycle regulation, and thereby demonstrated that the downregulation of miR-31 disrupts cellular homeostasis and contributes to the evolution and progression of prostate cancer. [score:7]
Therefore, to validate the expression of miR-31 in liver cancer, we observed miR-31 expression in the large cohorts of HCC patients available from the National Center for Biotechnology Information (NCBI) and Gene Expression Omnibus (GEO) database (accession numbers GSE21362 and GSE39678), and the data were presented as scatter plots. [score:7]
Taken together, we present evidences that miR-31 functions as a tumor suppressive miRNA by directly regulating HDAC2 and CDK2 expression in liver cancer progression. [score:7]
For example, miR-31 was demonstrated that overexpression of miR-31 led to increased growth rate by targeting suppressors, LATS2 and PPP2R2A in lung cancer [22]. [score:7]
Although we showed that ectopic miR-31 elicited inhibition of cellular growth of liver cancer cells through targeting HDAC2, it is necessary to prove that ectopic overexpression of 3′ UTR- deleted HDAC2 plasmid (pME18s-HDAC2-FLAG) can rescue the effects on cell cycle molecules in the same cells. [score:7]
Our results showed that ectopic expression of miR-31 resulted in suppression of HDAC2 and CDK2 protein expression in liver cancer cells. [score:7]
These results suggest that the expression of miR-31 is suppressed in HCC and its low expression associates with biological process of tumorigenesis and poor prognostic signs of HCC patients. [score:7]
Expression of miR-31 correlates inversely with breast cancer progression in humans, where an increase in expression of miR-31 target genes was observed as tumors progressed to more aggressive forms. [score:7]
Although the underlying mechanism leading to the suppression of miR-31 should be clearly elucidated, these epigenetic alterations cause the down-regulation of miR-31 and thereby contribute to the hepatocellular malignant transformation and proliferation. [score:6]
For instance, miR-31 was significantly down-regulated in breast cancer and bladder cancer, thus expression of miR-31 was inversely correlated with metastasis and aggressiveness [10, 11]. [score:6]
To clarify that expression of miR-31 is regulated by EZH2, cells were treated with DZNep (3-Deazaneplanocin A, an inhibitor of S-adenosylmethionine -dependent methyltransferase, and stimulates degradation of EZH2). [score:6]
It was found that miR-31 was able to suppress reporter gene activity in these cells, whereas mutants plasmids showed no changes in the reporter gene activity in both SNU-449 and SKHep-1 cells indicating miR-31 selectively regulate both HDAC2 and CDK2 expressions in HCC cells in vitro (Fig. 2D). [score:6]
Notably, we also observed that targeted-disruption of HDAC2 recapitulated the effect of ectopic miR-31 expression on the same molecules whereas CDK2 knockdown did not affect. [score:6]
Earlier report showed that miR-31 is located at the chromosome 9q21.3, and this locus is very close to the locations of tumor suppressors, CDKN2A and CDKN2B, that is frequently deleted in many cases of cancers, which may result in down-regulation of miR-31 [27, 28]. [score:6]
Unlikely with previous observation in liver cancer study, miR-31 expression was significantly down-regulated in these two different HCC cohorts (Fig. 1A). [score:6]
Our data, contradictive with previous observation, indicated that miR-31 expression was significantly down-regulated in patients with HCC. [score:6]
Next, to better understand the underlying mechanism of the growth inhibition elicited by miR-31, western blot analysis was performed for cell cycle regulatory proteins and miR-31 -targeting molecules, HDAC2 and CDK2. [score:6]
Ectopic expression of miR-31 elicits a tumor-suppressor effect by regulating cell-cycle proteins in liver cancer cells. [score:6]
MiR-31 inhibits liver cancer cell growth by targeting G1/S transition regulatory molecules. [score:5]
Figure 3(A) Ectopic expression of miR-31 suppressed SNU-449 and SKHep-1 cell proliferation. [score:5]
The direct target molecules of miR-31, HDAC2 and CDK2, as well as the cell cycle regulators and EMT markers, were analyzed with immunoblotting. [score:5]
In addition, Kaplan-Meier survival curves of patients with HCC indicated that the 5-year overall survival (OS) rates of HCC patients with low miR-31 expression was significantly lower than that of HCC patients with high miR-31 expression (Fig. 1B). [score:5]
As shown in Fig. 2B, Dicer knockdown augmented HDAC2 and CDK2 protein expressions in SNU-449 and SKHep-1 cells, whereas co-transfection of miR-31 mimics attenuated Dicer knockdown effect on the same cells. [score:5]
Interestingly when we performed prediction analysis of putative miR-31 targets by using miRWALK database, 399 genes were resulted in possible targets of miR-31. [score:5]
MiR-31 is well known metastatic suppressor by direct targeting integrin family, RhoA and RDX in various cancers but unknown in liver cancer [14]. [score:5]
Since EZH2, a core component of polycomb repressive complex2 (PRC2), was reported to be over-expressed in HCC, we assumed that hyper-methylation of H3 Lys-27 residue may be related with the suppression of miR-31 [20]. [score:5]
Notably, treatment of DZNep elicited remarkable suppression of EZH2, HDAC2 and CDK2 proteins with concomitant increase of miR-31 expression in SNU-449 and SKHep-1 cells (Fig. 6B and C). [score:5]
The phenotype caused by aberrant miR-31 expression seems to be strongly dependent on the endogenous expression levels. [score:5]
MiR-31 is aberrantly down-regulated in HCC and its expression is associated with the poor prognosis of patients with HCC. [score:5]
In colorectal cancer, it was demonstrated that miR-31 plays a significant role in activating the RAS signaling pathway through the inhibition of RASA1 translation, thereby improving colorectal cancer cell growth and stimulating tumorigenesis [24]. [score:5]
Thus, suppressive function of miR-31 on EMT molecules seems to be indirect effect of miR-31, and HDAC2 may also contribute to selective regulation of these EMT molecules. [score:5]
In the present study, we demonstrated that miR-31 functions as a tumor suppressor in the development of HCC by negative regulation of the major components in the cell cycle transition and EMT processing of cancer cells. [score:5]
Notably we also found that treatment of DZNep elicited remarkable suppression of EZH2, HDAC2 and CDK2 proteins with concomitant increase of miR-31 expression in liver cancer cells (Fig. 6B-E). [score:5]
Thus, to identify miR-31 target genes, we used the target prediction program, miRWALK (http://www. [score:5]
Notably we also able to generalize the repressive status of miR-31 expression in HCC by recapitulating miR-31 expression from the various large cohorts of HCC patients that are available from the NCBI, GEO database (Fig. 1). [score:5]
Ectopic expression of miR-31 potentially suppressed cell growth via transcriptional inactivation of HDAC2 and CDK2. [score:5]
The liver cancer cell lines, SNU-449 and SKHep-1, were treated with indicated drug (01% DMSO or 10 μM of 5-aza-dC), or transfected with siRNA (negative control siRNA, si- DNMT1), and analyzed protein expressions of miR-31 target genes, HDAC2 and CDK2. [score:5]
These results demonstrate that miR-31 is a direct regulator of endogenous expression HDAC2 and CDK2 in liver cancer cells. [score:5]
Ectopic expression of miR-31 increased the oncogenic potential of head and neck squamous cell carcinoma cells under normoxic conditions in cell culture or tumor xenografts by impeding factor-inhibiting hypoxia-inducible factor [23]. [score:5]
For example, miR-31 down-regulation has been detected in several other malignancies, such as bladder, esophageal, ovarian, and prostate cancer as well as in glioma, leukemia, melanoma, and mesothelioma. [score:4]
Here we report that miR-31 functions as a tumor suppressor through the regulation of cell cycle and epithelial-mesenchymal transition (EMT) proteins in hepatocarcinogenesis. [score:4]
MiR-31 regulates metastatic potential of liver cancer cells and is suppressed by deregulation of epigenetic modifiers. [score:4]
From this, all 9 HCC tissues exhibited significantly down-regulation of miR-31 in HCC (Fig. 1C). [score:4]
In addition to breast cancer, not only that miR-31 acted as a metastatic suppressor by regulating these genes, but also elicited cell cycle arrest and apoptosis in lung cancer [25]. [score:4]
si- HDAC2 and si- CDK2 were used for knockdown of miR-31 target genes, respectively. [score:4]
Thus, to support our hypothesis that HDAC2 and CDK2 expressions are regulated by miR-31 in HCC cell lines, we introduced Dicer specific siRNAs to block miRNA biogenesis in HCC cells. [score:4]
The anti-growth effect could be partially explained by the disruption of cell growth regulation on miR-31 targeting, such as cell cycle arrest, cellular senescence or apoptosis. [score:4]
These results demonstrate that miR-31 regulates cell cycle molecules through the selective control of HDAC2 expression in liver cancer cells. [score:4]
Next, to verify that miR-31 specifically binds to 3′UTRs of CDK2 and HDAC2 to interfere translation of those transcripts, mutant vectors harboring random mutation sequences of miR-31 biding sites of the 3′UTR of CDK2 and HDAC2 genes were generated, and then each vector was co -transfected with miR-31 into SNU-449 and SKHep-1 cells. [score:4]
A modified Boyden chamber assays revealed that ectopic expression of miR-31 mimics significantly suppressed chemoattractant (5% fetal bovine serum)-stimulated migratory and invasive responses of both SNU-449 and SKHep-1 cells, whereas AS-miR-31 co-transfection significantly rescued anti-migratory and invasion effects in the same cells (Fig. 4A and B). [score:4]
Thus, we next explored the effects of miR-31 overexpression on cell death and cell cycle regulation. [score:4]
Interestingly, in a subset of HCCs defined by Edmondson grade I (TG1, n = 5), grade II (TG2, n = 5), grade III (TG3, n = 6), miR-31 was gradually down-regulated in the progression of liver cancer (Fig. 1A, GSE39678). [score:4]
In another study, it was identified that WAVE3, actin cytoskeleton regulating molecule, was shown to be directly regulated by miR-31 [26]. [score:4]
Hence, the functional role of miR-31 is extremely complex and miR-31 can hold both tumor suppressive and oncogenic roles in different tumor types. [score:3]
MiR-31 is among the most frequently altered miRNAs in human cancers and altered expression of miR-31 has been detected in a large variety of tumor types. [score:3]
However, N-cadherin, E-cadherin, vimentin and fibronectin were not found as miR-31 target genes (data not shown). [score:3]
MiR-31 is down-regulated in hepatocellular carcinoma. [score:3]
In addition, overexpression of miR-31 mimics significantly abolished metastatic potential of HCC cells. [score:3]
Flow cytometric cell cycle analysis indicated that miR-31 overexpression led to an increase in the number of cells in the G1 phase with a concomitant decrease in the number of cells in the S phase and G2/M phase, but AS-miR-31 co-transfection attenuated this effect in the same cells (Fig. 3B). [score:3]
However, authors concluded that high level of miR-21, miR-31, miR-122, and miR-221 expression was correlated with cirrhosis but only miR-21 and miR-221 were associated with tumor stage. [score:3]
In some cases, such as colon cancer and oral cancer, miR-31 was highly over-expressed [12, 13]. [score:3]
In many different types of cancers, repressed miR-31 expression was demonstrated to contribute malignant transformation and proliferation of cancer cells. [score:3]
For liver cancer, the only one study reported that miR-31 was over-expressed, but no correlation with clinicopathlogical features was found [15]. [score:3]
In contrast, the suppressive effect of miR-31 on EMT molecules in liver cancer cells was significantly rescued by the con-transfection of AS-miR-31. [score:3]
The expression of miR-31 was normalized to U6 snRNA (* P<0.05; ** P<0.005, Student's t test) (D) The qRT-PCR analysis of miR-31 for hepatocellular carcinoma cell lines (n=7) and liver normal cell lines (n=2) (** P<0.005; *** P<0.001, Student's t test). [score:3]
To gain further insight into the regulatory effect of miR-31 on EMT, western blot analysis was performed for the EMT regulatory proteins in in liver cancer cells. [score:3]
In prostate cancer, hyper-methylation of miR-31 promoter was responsible for its low expression and contributed tumorigenesis [21]. [score:3]
MiR-31 regulates HDAC2 and CDK2 expression by binding 3′-UTR in hepatocellular carcinoma. [score:3]
Then, to determine whether HDAC2 and CDK2 are selectively regulated by miR-31 via direct interaction with the 3′-UTR of these genes, we cloned the 3′-UTR of HDAC2 and CDK2 into a reporter vector linking the luciferase open reading frame downstream to generate psi-CHECK2-HDAC2_3′-UTR and psiCHECK-CDK2_3′-UTR plasmid, respectively (Fig. 2C and Supplementary Fig. S1). [score:3]
Furthermore, even though expression of miR-31 and its functions were extensively studied and well defined in many cancers, the role of miR-31 in human liver cancer is still unidentified. [score:3]
The expression of miR-31 varies from one cancer to another and thus its functional role is very diverse in different malignancies. [score:3]
In contrast, overexpression of miR-31 in MIHA and L-O2 (immortalized normal hepatic cell lines) did not effect on cell growth rates of these two different cell lines (Supplementary Fig. S2). [score:3]
Inactivation mechanism of tumor suppressor miR-31 in liver cancer. [score:3]
The five year survival rate was significantly decreased in patient with low level of miR-31 expression in the tumor tissues (Log-rank P = 0.0015*) (C) The qRT-PCR analysis for 9 paired HCC tissues. [score:3]
These results provide the underlying mechanisms leading to the suppression of endogenous miR-31 in HCC. [score:3]
Thus, the aberrant expression of these miRNAs, such as miR-31 and -122 remained to be validated in liver cancer. [score:3]
On the contrary to this, miR-31 was also reported as a tumor suppressor in other type of cancers. [score:3]
In breast cancer, miR-31 was under expressed in metastatic tumor and negatively correlated with high risk of metastasis. [score:3]
However, increased expression of miR-31 has also been detected for example in colorectal, lung and pancreatic cancer, head and neck squamous cell carcinoma, and osteosarcoma [14]. [score:3]
From this database, at least in six out of eight different prediction programs, 399 genes were predicted to be targeted by miR-31 (data not shown). [score:3]
Next, to verify the suppression of miR-31 in HCC patients, miR-31 expressions of 9 randomly selected HCC tissues paired with adjacent non-cancerous liver tissues were investigated by quantitative real-time PCR (qRT-PCR). [score:3]
Our results demonstrated that repression of miR-31 contributes to transcriptional activation of HDAC2, and, thereby causes the acceleration of cell cycle transition of cancer cells through selective regulation of cell cycle components (Fig. 3). [score:2]
Next, to investigate biological functions of miR-31 in hepatocellular malignant proliferation and transformation, we attempted ectopic expression of miR-31 and studied in the 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenytetrazolium bromide (MTT) assay for the measurement of cell growth rate of two different liver cancer cell lines, SNU-449 and SKHep-1. Ectopic overexpression of miR-31 resulted in reduced growth rates of these two different liver cancer cell lines, whereas co-transfection with AS-miR-31 (an antisense inhibitor of miR-31) significantly blocked this anti-growth effect (Fig. 3A). [score:2]
In vivo validation of miR-31 regulating molecules in DEN -induced rat liver cancer mo del. [score:2]
Figure 5 In vivo validation of miR-31 regulating molecules in DEN -induced rat liver cancer mo del(A) Macroscopic observation of the whole liver from the DEN -induced rat mo del (arrows; tumors). [score:2]
MiR-31 is one of well identified miRNAs in cancer biology, and interestingly, regulation patterns and functions of miR-31 were diverse depending on cancer types. [score:2]
However, miR-31 overexpression showed no significant induction of apoptotic cells compared to miRNA control (Fig. 3C). [score:2]
Although further research is required to identify regulatory mechanisms for the repression of miR-31 in liver cancer, the results suggest that the miR-31 may play a central role in hepatocellular malignant transformation and proliferation providing novel therapeutic intervention of liver malignancy. [score:2]
MiR-31 was significantly down-regulated compared to corresponding non-tumor tissue. [score:2]
For mutagenesis of the miR-31 -binding site, a QuickChange site-directed Mutagenesis Kit (Agilent Technologies, Palo Alto, CA) was used according to the manufacturer's instructions. [score:2]
These results suggest that anti-metastatic potential of miR-31 could be attributed to the selective regulation of EMT proteins in liver cancer cells. [score:2]
The human liver cancer cell lines (Hep3B, Huh7, PLC/PRF/5, SK-Hep-1, SNU-182 and SNU-449) exhibited relatively low miR-31 expression levels compared to that of non-cancer cell lines (MIHA and L-O2). [score:2]
In parallel with our previous observation, miR-31 selectively regulated EMT proteins, N-cadherin, E-cadherin, vimentin and fibronectin, to control metastatic potential of liver cancer cells (Fig. 4). [score:2]
MiR-31 suppressed motility and invasion of HCC cells. [score:2]
From this, obviously miR-31 is appeared to be suppressed in HCC compared with that of non-cancerous surrounding tissues. [score:2]
Wild type or mutant 3′-UTR construct of HDAC2 and CDK2 were cloned into a psi-CHECK2 vector, respectively, and co -transfected with miR-31 mimics in SNU-449 and SKHep-1 cells. [score:1]
The levels of HDAC2 and CDK2 in the Bio-miR-31 pull-down were quantified by qRT-PCR. [score:1]
Transfection of antisense miR-31 (AS-miR-31) attenuated anti-growth effect of miR-31. [score:1]
We then stained the cells with annexin V-FITC and PI after transfection of miR-31 mimics for apoptosis analysis. [score:1]
In addition, to clarify the direct interaction between miR-31 and 3′-UTRs of the two transcripts, we carried out biotin-labeled RNA pull-down assays. [score:1]
In similar, when ras-transformed NIH-3T3 cells were transfected with miR-31 mimics to generalize the effect of miR-31 in the regulation of metastatic potential, we obtained consistent results in both motility and invasion assays (Supplementary Fig. S3). [score:1]
Notably, N-cadherin, vimentin and fibronectin, hallmarks of EMT, were dramatically decreased in miR-31 mimics transfectants, whereas E-cadherin, an epithelial markers, was increased in both SNU-449 and SKHep-1 cells (Fig. 4C and D). [score:1]
Figure 4(A) of liver cancer cells transfected with miR-31 or co -transfected miR-31 with AS-miR-31. [score:1]
Thus, it is assumed that miR-31 has a specific function in each type of malignancy, and several mechanisms, including methylation -dependent silencing and local deletion, may explain its different roles in different tumor types. [score:1]
Small interfering RNAs (siRNAs) of Dicer (sense: 5′-UAAAGUAGCUGGAAUGAUG-3′, antisense: 5′-CAUCAUUCCAGCUACUUUA-3′), CDK2 (sense: 5′-GGAGCUUGUUAUCGCAAAU, antisense: 5′-AUUUGCGAUAACAAGCUCC-3′), DNMT1 (sense: 5′-CACUGGUUCUGCGCUGGGA-3′, antisense: 5′-UCCCAGCGAGAACCAGUG-3′) and microRNA mimics of miR-31 (sense: 5′-AGGCAAGAUCUGGCAUAGCU-3′, antisense: 5′-AGCUAUGCCAGAUCUUGCCU-3′) were synthesized by Genolution (Seoul, Korea). [score:1]
In contrast, this result was significantly attenuated by the co-transfection of AS-miR-31 in the same cells (Fig. 3D). [score:1]
However, little is known about the miR-31 status in patients with HCC and the possible roles in hepatocarcinogenesis. [score:1]
SNU-449 and SKHep-1 cells were transfected with miR-31 mimics after transfected with Dicer siRNA or negative control siRNA (N. C). [score:1]
In previous studies, miR-31 was reported as an oncomir in several human cancers. [score:1]
On the other hand, hyper-methylation of miR-31 promoter region was also reported as inactivating mechanism for miR-31 in prostate cancer [21]. [score:1]
Thus, functional role of miR-31 in liver cancer is elusive and to be uncovered. [score:1]
SNU-449 and SKHep-1 cells were transfected with Biotin-labeled microRNA control (Bio-N. C) or Biotin-labeled miR-31 mimics for 48 hours. [score:1]
Additionally, endogenous expression of miR-31 was investigated by qRT-PCR in nine different liver cell lines, including immortalized normal hepatic cell lines (Fig. 1D). [score:1]
To be specific, ectopic miR-31 repressed metastatic potential and this result was explained by miR-31 -mediated repression of ITGA5, RDX and RhoA [10]. [score:1]
SNU449 and SKHep-1 cells were transfected with Bio-miR-31 or Bio-miR-control in two 60mm dishes. [score:1]
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[+] score: 124
This data on miR-31 directed Tfrc transcript down-regulation is also consistent with the gene expression microarray analyses, in which both Tfrc and miR-31 were up-regulated during enamel maturation. [score:10]
The most immediate response from cells to fine-tune this Tfrc transcriptional up-regulation may be to activate processes that target Tfrc mRNAs for degradation, which may include gene up-regulation of miR-31 transcription. [score:9]
MiRNA mimics and inhibitors for miR-153 and miR-31 were also mouse-specific and were obtained from Qiagen (Catalog # MSY0000163-miR-153 mimic, MIN0000163-miR-153 inhibitor, MSY0000538-miR-31 mimic, MIN0000538-miR-31 inhibitor). [score:7]
In our efforts to validate the regulatory relations between Lamp1 and miR-153, as well as between Tfrc and miR-31, we first demonstrated the coexpression of miRNAs and mRNAs of target genes during maturation-stage development. [score:7]
In human natural regulatory T cell FOXP3 expression is affected by both miR-21 and miR-31, although the regulation of miR-21 is indirect [52]. [score:6]
MiR-21, miR-31 and miR-488 are down-regulated, while miR-153, miR-135b, miR-135a and miR-298 are up-regulated in secretory-stage enamel formation compared to maturation-stage. [score:6]
Further, we used luciferase reporter assays to provide evidence that two of these differentially expressed miRNAs, miR-153 and miR-31, are potential regulators for their predicated target mRNAs, Lamp1 (miR-153) and Tfrc (miR-31). [score:5]
For example, miR-21 and miR-31 facilitate invasion and metastasis of colon carcinoma cells by suppressing the same target TIAM1 in TGF-β signaling pathway [51]. [score:5]
The expression levels of miR-153 and miR-31 in LS8 cells at different time points, following the transfection of corresponding miRNA mimics or inhibitors, were first checked separately using quantitative real-time PCR. [score:5]
The interaction between the seeding sequence of the miRNA (miR-153 and miR-31) and the 3′-UTR of the target mRNA (Lamp1 and Tfrc) was predicted by TargetScan, and the binding site of miR-31 to the mRNA of Tfrc was predicted to be highly conserved across vertebrates. [score:5]
The effects of miR-153 and miR-31 on target proteins (Lamp1 and Tfrc respectively) was identified indirectly by the changes in luciferase reporter assays induced by exogenously introduced mimics and inhibitors of corresponding miRNAs into the host cells (Figures  7B and 8B). [score:5]
The changes in the expression of intracellular miR-31 were relatively subtle following transfection with miR-31 mimics, while the introduction of miR-31 inhibitors repressed the intracellular miR-31 almost immediately (within 10 min) after transfection. [score:5]
One of the miRNAs identified as being highly up-regulated in maturation-stage enamel organ cells is miR-31 (~10 fold increase when compared to secretory-stage), and bioinformatic prediction identifies miR-31 as a potential regulator of Tfrc in all vertebrate genomes. [score:4]
For miR-31 (mature miRNA sequence: 5′-AGGCAAGAUGCUGGCAUAGCUG-3′) and Tfrc, the experimental groups involved LS8 cells: 1) transfected with luciferase reporter vector (Tfrc 3′-UTR); 2) co -transfected by miR-31 mimics and luciferase reporter vector (Tfrc 3′-UTR); 3) co -transfected by miR-31 inhibitors and luciferase reporter vector (Tfrc 3′-UTR). [score:3]
That is, miR-140, miR-31, miR-875-5p and miR-141 were expressed mainly during tooth morphogenesis identified at embryonic day 16 (E16), whereas miR-689, miR-720, miR-711 and miR-455 were prevalent at the cytodifferentiation stage (E18) [8]. [score:3]
Seven differentially expressed miRNAs (miR-21, miR-31, miR-488, miR-153, miR-135b, miR-135a and miR298) in secretory- and/or maturation-stage enamel organs were confirmed by in situ hybridization. [score:3]
The intracellular miR-31 level following transfection with the miR-31 inhibitors remained undetectable for the 48 h of observation. [score:3]
In the case of Tfrc and miR-31, the highest levels of expression of both were noted in maturation-stage amelogenesis (Additional files 1, 2 and 19). [score:3]
For the data presented, the amount of luciferase reporter vector used was fixed at 700 ng, and the concentrations of miR-31 mimics and inhibitors in final transfection complex were 20 pM and 0.2 nM respectively. [score:3]
When miR-31 inhibitors were added to Tfrc 3′-UTR LS8 cells there was a 77.8% increase in luciferase reporter activities (P = 0.008) (Figure  8B). [score:3]
Taken together these results would suggest that the Tfrc 3′-UTR luciferase vector is functional, and that the miR-31 mimics effectively target the Tfrc transcript. [score:3]
This may suggest that the initial levels of endogenous miR-31 are so high that the targeting activity of exogenous miR-31 mimics on the 3′-UTR of Tfrc is minimal. [score:3]
Exogenously added miR-31 mimics showed a small inhibitory effect, however it was not statistically significant (P = 0.284) (Figure  8B). [score:3]
Figure 8 Tfrc is the potential target of miR-31. [score:3]
By comparison, a higher level of intracellular miR-31 was detected in LS8 cells before transfection with miR-31 mimics, indicating that miR-31 was intrinsically expressed in LS8 cells (Figure  8A). [score:3]
The expression patterns of seven selected miRNAs (miR-21, miR-31, miR-488, miR-153, miR-135b, miR-135a and miR-298) were examined (Figure  6E-R). [score:3]
As a result, we decided to use miR-31 for subsequent in vitro verification that Tfrc could be subjected to miRNA regulation at some level in the mouse genome. [score:2]
Prior to luciferase reporter assays, the levels of miR-153 and miR-31 in LS8 cells were detected using miRNA real-time PCR analysis at different time points: 0 h, 6 h, 24 h and 48 h following transfection by miRNA mimics or inhibitors. [score:2]
In situ hybridization analyses of miR-21, miR-31 and miR-488 generated higher signal intensities in maturation-stage enamel organ cells than in secretory-stage enamel organ cells (Figures  6E and 4J), and this data correlates well (same directional change) with the miRNA qPCR array data/fold increase (i. e., miR-21, miR-31, miR-488 increased by 5.2, 9.5 and 6.9 fold, respectively) (Additional file 1). [score:2]
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[+] score: 100
That the tumor suppressor genes Fxbw7, Pdcd4, and Stk40 were downregulated at the mRNA and protein level in marked-ZD tumor group (Figure 6) and that they were predicted to interact to alter network of target proteins [65, 66, 77] (Figure 7) provide support that miR-223, miR-21, and miR-31 have an important role in ESCC and may be useful prognostic biomarkers and therapeutic targets for ESCC. [score:10]
Analysis of esophageal expression of Fbxw7, Stk40, and Pdcd4 (respective tumor suppressor targets of miR-223, miR-31, and -21) in Zn-modulated rats at tumor endpoint. [score:7]
That the three tumor suppressor targets are predicted to interact to alter network of cancer-related proteins [65, 66, 77] provide support that miR-223, miR-21, and miR-31 have an important role in ESCC and may be useful therapeutic targets in ESCC. [score:7]
We selected 8 miRNAs in ZD3T esophageal tissue (miR-223, -21, -31, -146a, -146b, -221, -194, and -106b) and two miRNAs (miR-31, -223) in ZD6T and ZD12T esophageal tissues, Figure 4B shows that the Taqman data confirmed the upregulation of all 8 selected miRNAs in ZD3T vs ZST samples, and the upregulation of miR-223 and miR-31 in ZD6T and ZD12T samples. [score:7]
Figure 7 A. The displayed esophagus-specific nine-gene network shows predicted functional relationships among the genes that are most functionally related to Stk40, Pdcd4 and Fbxw7 (tumor-suppressor targets of miR-31, mir-21 and miR-223, respectively). [score:5]
miR-223, miR-21, and miR-31 can target many important tumor suppressor genes, including FXBW7 [25, 61], STK40 [60, 62, 63], and PDCD4 [64]. [score:5]
Notably, miR-31 and miR-146a were differentially expressed in ZD6/ZD12 esophagus as they were in ZD3 esophagus, albeit at a lower expression level. [score:5]
A. The displayed esophagus-specific nine-gene network shows predicted functional relationships among the genes that are most functionally related to Stk40, Pdcd4 and Fbxw7 (tumor-suppressor targets of miR-31, mir-21 and miR-223, respectively). [score:5]
STK40 is a known negative regulator of NF-κB mediated transcription [90] and a miR-31 direct target [60, 62, 63]. [score:5]
miR-223, miR-21, and miR-31 are the top -upregulated species in the high ESCC-burden, marked-ZD esophagus. [score:4]
The signature was defined by five top up-regulated oncogenic miRNAs (miR-31, -223, -21, -146b, -146a) [15, 16, 22– 26, 29, 30, 34, 58] that were up 4.9-3.7 fold. [score:4]
In addition, prolonged ZD by itself induced an oncogenic microRNA (miRNA) signature with miR-31 as the top upregulated species [14], a feature of human ESCCs as well [15, 16]. [score:4]
Our study suggests that miR-223, miR-31 and miR-21 alone or in combination could be used as therapeutic targets for treatment of ESCC. [score:3]
Thus, moderate and mild-ZD induces alterations in miRNA expression, including miR-31 and miR-223. [score:3]
Cellular localization of miR-223, miR-31 and miR-21 expression in human ESCC tissue. [score:3]
These findings show that moderate and mild-ZD induces alterations in miRNA expression, including miR-31 and miR-146a. [score:3]
Using the nanoString platform, miRNA expression profiles distinguished the highly preneoplastic/proliferative marked-ZD esophageal phenotype with a 5-miRNA signature (miR-31, -223, -21, -146b, -146a), from the less proliferative, mild-ZD phenotype with a 3-miRNA signature (miR-146a, -31, -223). [score:3]
In addition, miR-223 and miR-31 dysregulation is common to marked-ZD and moderate/mild-ZD tumor groups (Figure 4A). [score:2]
Recently, we demonstrated by ChIP-seq analysis that in ZD esophagus, the miR-31 promoter region and NF-κB binding site were activated, unleashing miR-31 -associated STK40-NF-κB controlled inflammatory signaling to produce a preneoplastic phenotype; Zn-replenishment restores the normal regulation of this genomic region and a normal esophageal phenotype [60]. [score:2]
All 12 cases showed intense to moderate miR-31, miR-223, and miR-21 ISH signal in near serial sections of moderately to poorly differentiated ESCC tumor samples (Figure 5). [score:1]
Following deparaffinization, rehydration in graded alcohol and proteinase K treatment, tissue sections were hybridized with miR-31 probe (20 nM), miR-223 or miR-21 probe (50 nM) in hybridization buffer (Exiqon) at 50°C - 57°C for 14 h in a hybridizer (Dako, Glostrup, Denmark). [score:1]
Localization of miR-223, miR-31, and miR-21 in human esophageal squamous cell carcinoma (ESCC) tissue by in situ hybridization (ISH). [score:1]
Among which, miR-31 [15, 16, 30, 60] and miR-223 [25, 26, 34] are oncomiRs for human ESCC. [score:1]
miRCURY locked nucleic acid (LNA)™ microRNA detection probes, namely, rno-miR-21, rno-miR-31, rno-miR-223, hsa-miR-31, hsa-miR-223, negative controls (rno-miR-31) with mismatches at two position, were purchased from Exiqon (Vedbaek, Denmark). [score:1]
A Venn diagram (Figure 4A) showed that miR-31, -223, -7i, -543 were the four common miRNAs shared among ZD3T, ZD6T and ZD12T esophagus. [score:1]
Figure 4 A. Venn diagram showing miR-223 and miR-31 are common to ZD3T, ZD6T, and ZD12T esophagi (cutoff point of P < 0.05 and fold difference >1.3), and scatterplot showing their fold change vs ZST. [score:1]
A limitation of this study is the fact that the underlying biological mechanisms of the key dysregulated miRNAs in ESCC development, namely, miR-223, miR-21, and miR-31, were not investigated. [score:1]
In situ hybridizationmiRCURY locked nucleic acid (LNA)™ microRNA detection probes, namely, rno-miR-21, rno-miR-31, rno-miR-223, hsa-miR-31, hsa-miR-223, negative controls (rno-miR-31) with mismatches at two position, were purchased from Exiqon (Vedbaek, Denmark). [score:1]
A. Venn diagram showing miR-223 and miR-31 are common to ZD3T, ZD6T, and ZD12T esophagi (cutoff point of P < 0.05 and fold difference >1.3), and scatterplot showing their fold change vs ZST. [score:1]
Previously, we demonstrated an abundant miR-31 ISH signal in human ESCC tissue [60]. [score:1]
miR-31 acts as an oncomiR in squamous cell carcinomas (SCCs), including ESCC [15, 16], tongue SCC [87], head and neck SCC [88], and skin SCC [89]. [score:1]
B. Validation of eight representative miRNAs in ZD3T esophagus; and miR-223 and miR-31 in ZD6T and ZD12T esophagi. [score:1]
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4
[+] score: 63
Among those seventeen deregulated miRNAs miR-31 was up-regulated on day 2, day 7 and day 14. miR-199a was up-regulated on day 7 and day 14. miR-214 was up-regulated on day 7 and day 14. miR-499 was down-regulated on day 2 and day 7. Table 1 miRNAs differentially expressed in the myocardial tissues of rats with acute myocardial infarction. [score:16]
Among those seventeen deregulated miRNAs miR-31 was up-regulated on day 2, day 7 and day 14. miR-199a was up-regulated on day 7 and day 14. miR-214 was up-regulated on day 7 and day 14. miR-499 was down-regulated on day 2 and day 7. Table 1 miRNAs differentially expressed in the myocardial tissues of rats with acute myocardial infarction. [score:16]
Expression levels of miR-126 and miR-499 were greatly down-regulated after AMI, whereas expression levels of miR-31 and miR-214 increased after AMI (Figure 3 and Additional File 4). [score:8]
On day 7, miR-31, miR-214, miR-199a-5p, and miR-199a-3p were up-regulated, whereas miR-181c, miR-29b, miR-26b, miR-181d, mir-126, mir-499-5p, and miR-1 were down-regulated. [score:7]
On day 2, miR-31, miR-223, miR-18a, and miR-18b were up-regulated, whereas miR-451 and miR-499-5p were down-regulated. [score:7]
On day 14, miR-214, mir-923, miR-711, and miR-199a-3p, and miR-31 were up-regulated, of which miR-31 showed the most striking up-regulation (an increase of eight-fold compared with the sham-control). [score:6]
miRNA Tissues in which miRNA is most highly expressed tissueDay 2(Fold change/Q-value)Day 7(Fold change/Q-value)Day 14(Fold change/Q-value) miR-31 Colon4.504/0.000 [#]5.923/0.000 [#]8.224/0.000 [#] miR-18a Small intestine2.136/0.013 [#] 1.016/0.507 0.904/0.612 miR-18b Small intestine2.045/0.000 [#] 1.502/0.023 1.314/0.000 miR-214 Distal colon 1.970/0.0002.992/0.000 [#]2.404/0.000 [#] miR-223 Spleen4.063/0.013 [#] n/a n/a miR-923 n/a 1.461/0.160 n/a2.232/0.000 [#] miR-711 n/a n/a n/a2.542/0. [score:3]
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5
[+] score: 37
The results demonstrated that in the hypertonic dialysate group, miR-31, miR-93, miR-100, miR-152, miR-497, miR-192, miR-194 and miR-200b were all significantly down-regulated whereas miR-122 was highly up-regulated (all P <0.05) (Figure  3). [score:7]
The miRNA screen identified 8 significantly down-regulated miRNAs (miR-31, miR-93, miR-100, miR-152, miR-497, miR-192, miR-194 and miR-200b) and one highly up-regulated miRNA (miR-122) in the hypertonic dialysate group. [score:7]
It was found that 8 miRNAs were significantly and consistently down-regulated in the hypertonic dialysate group (miR-31, miR-93, miR-100, miR-152, miR-497, miR-192, miR-194 and miR-200b), and within which miR-192, miR-194 and miR-200b were also down-regulated in the normal saline group (Table  3). [score:7]
Compared with the control and saline groups, both miRNA microarray and real-time PCR analyses demonstrated that miR-31, miR-93, miR-100, miR-152, miR-497, miR-192, miR-194 and miR-200b were significantly down-regulated, and miR-122 was highly up-regulated in the hypertonic dialysate group. [score:6]
In a mouse mo del of pulmonary fibrosis, miR-31 was shown to be down-regulated in the fibroblasts [38]. [score:4]
These results provide us a clue to find out the targets of miR-31 in peritoneum. [score:3]
Furthermore, miR-31 was identified as a direct modulator of integrin-α(5) and RhoA, two critical activators of the migratory activity of fibroblasts [38]. [score:2]
Taken together, these results suggest to us that the miRNA species identified in our miRNA screen (mir-31, mir-93, mir-192, mir-194 and mir-200b) may be critical in the process of mesothelial cell EMT and in the progression of peritoneal fibrosis. [score:1]
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6
[+] score: 32
When we compared the mRNA and miRNA profiles, differentially regulated in PKD, with Argonaute (a comprehensive database on miRNAs; [45, 71]), there were few genes reported as miRNA target like tropomyosin 1, alpha (TPM1) as a target of miR-21, the beta polypeptide of tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein (YWHAB), regulatory subunit 9B of protein phosphatase 1 (PPP1R9B), early growth response 3 (EGR3) and dynamin 1-like (DNM1L) as targets of miR-31, plysia ras-related homolog A2 (RHOA) as targets of miR-217, etc. [score:10]
miRNA Target Genes Pathways miR-128 ABCB9, BTG1, DSCR1, RASD1 ABC transporters General miR-136 GRN, PPP1R9B miR-147 HOXA1, PTGFRN miR-148 EGR3, SCN3A miR-181b IGF1R, NKX6-1 Adherens junction, Maturity onset diabetes of the, Focal adhesion, **Long term depression miR-196a ABCB9, CPB2, IRS1, MAPK10 ABC transporters General, Complement and coagulation cas, Adipocytokine signaling pathwa, Insulin signaling pathway, Type II diabetes mellitus, Fc epsilon RI signaling pathwa, Focal adhesion, **GnRH signaling pathway, **MAPK signaling pathway, Toll like receptor signaling p, Wnt signaling pathway miR-203 SARA1 miR-20 BTG1, SARA1, YWHAB Cell cycle miR-21 TPM1 mir-216 GNAZ **Long term depression miR-217 RHOA Adherens junction, Axon guidance, Focal adhesion, Leukocyte transendothelial mig, Regulation of actin cytoskelet, TGF beta signaling pathway, T cell receptor signaling path, Tight junction, Wnt signaling pathway miR-31 ATP2B2, DNM1L, EGR3, PPP1R9B, YWHAB **Calcium signaling pathway, Cell cycle miR-7 SLC23A2 miR-7b HRH3, NCDN, SLC23A2 **Neuroactive ligand receptor in b: miRNAs and their targets (from TargetScan and miRanda). [score:8]
In line with the expression on the miRNA-arrays, in qPCR analysis (Figure 4), miR-31 was 3.15 fold down regulated in diseased samples compared to healthy tissue. [score:5]
We predict that several of the differentially regulated genes are miRNA targets and miR-21, miR-31, miR-128, miR-147 and miR-217 may be the important players in such interaction. [score:4]
Interestingly, the expressions of miR-31 and miR-217 have not been previously reported in kidney. [score:3]
It is interesting to note that miR-31 and miR-217 have not been previously reported in kidney. [score:1]
Furthermore, we describe some newly detected miRNAs, miR-31 and miR-217, in the kidney which have not been reported previously. [score:1]
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7
[+] score: 23
Divergent inverse correlation of miR-143 & HK2 expression in nonproliferative esophagus vs proliferative ZD esophageal neoplasia and human ESCCTo understand the distribution and localization of miR-143 in esophageal neoplasia in relation to localization of its target HK2 protein and the level of cell proliferation, we performed in situ hybridization (ISH) and immunohistochemical staining (IHC) on near serial sections of rat esophageal tissues (n = 10 rats/group), as well as in the archived human ESCC tissues for which we previously reported overexpression of miR-31, -21, -223 [27, 28]. [score:7]
Using the NanoString microRNA expression profiling platform, we showed that ZD promotes ESCC by inducing an oncogenic miRNA signature that resembles the human ESCC miRNAome [25] with up-regulation of oncogenic miR-31, -223, and -21 [26- 28]. [score:6]
To understand the distribution and localization of miR-143 in esophageal neoplasia in relation to localization of its target HK2 protein and the level of cell proliferation, we performed in situ hybridization (ISH) and immunohistochemical staining (IHC) on near serial sections of rat esophageal tissues (n = 10 rats/group), as well as in the archived human ESCC tissues for which we previously reported overexpression of miR-31, -21, -223 [27, 28]. [score:5]
Using the same human ESCC tissues in which we previously documented overexpression of miR-31, miR-21, miR-223 by ISH [28], Figure 4 shows these human ESCC tissues were also highly proliferative with numerous PCNA -positive nuclei (n = 12 cases). [score:3]
In situ hybridizationmiRCURY locked nucleic acid (LNA)™ microRNA detection probes, namely, hsa-miR-143, rno-miR-31, and negative controls were purchased from Exiqon (Vedbaek, Denmark). [score:1]
miRCURY locked nucleic acid (LNA)™ microRNA detection probes, namely, hsa-miR-143, rno-miR-31, and negative controls were purchased from Exiqon (Vedbaek, Denmark). [score:1]
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8
[+] score: 18
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-489, 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-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
MiRNAs found to be primarily down-regulated in DHT -treated rats includes rno-miR-770, rno-miR-466c, rno-miR-21, rno-miR-31, rno-miR-182, rno-miR-183, rno-miR-96, rno-miR-132, rno-miR-182, rno-miR-384-3p and rno-miR-184. [score:4]
Thus, it is possible that the down-regulation of miRNAs (rno-miR-770, rno-miR-466c, rno-miR-31, rno-miR-183, rno-miR-96, rno-miR-132, rno-miR-182, rno-miR-384-3p and rno-miR-184) observed in this study could be associated with promoted thecal hyperandrogenesis [37, 38]. [score:4]
Whereas rno-miR-24 and rno-miR-183 were highly expressed in the theca and, to a lesser extent, in the granulosa cells of the cystic follicles (Figure  5), Rno-miR-31 and rno-miR-96 were present in the cumulus granulosa cells. [score:3]
Among the fourteen miRNAs mapped to the ingenuity databases, twelve (rno-let-7d, rno-miR-132, rno-miR-182, rno-miR-183, rno-miR-184, rno-miR-21, rno-miR-221, rno-miR-24, rno-miR-25, rno-miR-26b, rno-miR-31 and rno-miR-96) had 171 experimentally validated targets. [score:3]
For example, rno-miR-96, rno-miR-31 and rno-miR-222 were exclusively expressed in the theca of cystic follicles. [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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[+] score: 14
Note that combination of hypoxia and UFP-512 treatment significantly altered the expression levels of miR-363*, -370, -21 and miR-31 in the cortex following 10-day treatment. [score:3]
Although UFP-512 treatment alone did not alter the miR-31 expression under normoxic conditions, it led to a 50% increase in miR-31 levels in the 1-day hypoxia background (Figure 6d). [score:3]
Relative miRNA expression levels of miR-363*, -370, -21 and miR-31 in the rat cortex following 1, 5 or 10 days of hypoxia with or without UFP-512 treatment. [score:3]
Under normoxic conditions, UFP-512 had no appreciable effect on the miR-31 levels after 1 or 5 days, however, after 10 days it repressed miR-31 expression by >60%. [score:3]
Following 5 days of UFP-512 treatment, miR-31 levels were unchanged in the normoxic cortex. [score:1]
Hypoxic conditions repressed miR-31 levels by 50 and 75% in the control and DOR activation backgrounds, respectively. [score:1]
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10
[+] score: 11
12 of these miRNAs were ≥50% up-regulated in both groups with particularly strong increases in expression for miR-199a, miR-21, miR-214, miR-221, miR-222, and miR-31 (Figure 2B). [score:6]
Several miRNAs, including miR-21, miR-27, miR-31, miR-199a, miR-214 and miR-222 were up-regulated in these mouse mo dels in the same directions and to similar extents as observed in this study [11], [18]. [score:5]
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11
[+] score: 8
Other miRNAs from this paper: hsa-mir-31, mmu-mir-31, rno-mir-31a, ocu-mir-31
Aberrant up-regulation of polycomb proteins contribute to miR-31 down-regulation epigenetically leading to activation of NF-κB and apoptosis resistance in ATL cells (Yamagishi et al., 2012). [score:7]
Polycomb -mediated loss of miR-31 activates NIK -dependent NF-κB pathway in adult T cell leukemia and other cancers. [score:1]
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12
[+] score: 8
Then, these HEK 293 cells were treated with vehicle, pDNR-CMV (an empty plasmid, 0.2 µg/ml), pmiR-382 (a plasmid expressing miR-382, 0.2 µg/ml) or pmiR-31 (a plasmid expressing miR-31, 0.2 µg/ml). [score:5]
The luciferase reporter construct, containing the putative miR-382 binding sequence from 3′-UTR of rat Drd1 gene, was transfected into HEK293 cells with vehicle (Vehicle), an empty vector (pDNR-CMV), miR-382 (pmiR-31) or a control plasmid expressing an unrelated miRNA, miR-31 (pmiR-31). [score:3]
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13
[+] score: 7
The 3′UTR of Tollip contains a miR31 binding site; miR31 binding inhibits translation [11]. [score:5]
Tollip is known to be post-transcriptionally regulated by other miRNAs, including miR-31 [11]. [score:2]
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14
[+] score: 7
Other investigators found that miR-31 targets the 3' UTR of Prox1 to suppress its expression in human lymphatic endothelial cells, and that over-expressed miR-31 led to defective lymphangiogenesis in Xenopus and zebrafish embryos [22]. [score:7]
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15
[+] score: 7
The following forward primers were designed to confirm the sequencing results of miRNAs that showed differential expression patterns: tsp-miR-100 5′-AAC CCG TAG ATC CGA ACT TGT GT-3′; tsp-let-7 5′-TGA GGT AGT AGG TTG TAT AGT T-3′; tsp-miR-228 5′-AAT GGC ACT GGA TGA ATT CAC GG-3′; tsp-miR-1 5′-TGG AAT GTA AAG AAG TAT GTA G-3′; tsp-miR-31 5′-AGG CAA GAT GTT GGC ATA GCT GA-3′; tsp-novel-108 5′-CTT GGC ACT GTA AGA ATT CAC AGA-3′; tsp-novel-83 5′-TTG AGC AAT TTT GAT CGT AGC-3′; tsp-novel-46 5′-TGG ACG GCG AAT TAG TGG AAG-3′; tsp-novel-86 5′-TGA GAT CAC CGT GAA AGC CTT T-3′; tsp-novel-21 5′-TCA CCG GGT AAT AAT TCA CAG C-3′. [score:2]
0026448.t001 The sequencing data showed that, of the 21 conserved miRNAs, tsp-let-7 and tsp-miR-87 were found to locate only in the 3′ arm of their pre-miRNAs, and tsp-miR-31 was located only in the 5′ arm of the hairpin structures. [score:1]
Alignment of the tsp -mir-31 sequence with homologues from other organisms. [score:1]
Five conserved miRNAs (tsp-miR-228, tsp-miR-100, tsp-let-7, tsp-miR-1 and tsp-miR-31) and five novel miRNAs (tsp-novel-108, tsp-novel-83, tsp-novel-46, tsp-novel-86 and tsp-novel-21) with relatively higher TPM values identified by sequencing were validated by qRT-PCR and Northern blot. [score:1]
0026448.t001The sequencing data showed that, of the 21 conserved miRNAs, tsp-let-7 and tsp-miR-87 were found to locate only in the 3′ arm of their pre-miRNAs, and tsp-miR-31 was located only in the 5′ arm of the hairpin structures. [score:1]
Figure 3 Alignment of the tsp -mir-31 sequence with homologues from other organisms. [score:1]
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16
[+] score: 4
Liu et al. reported that miR-31 is able to promote VSMC proliferation via down-regulation of LATS2, which is characterized as a tumour suppressor 32. [score:4]
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17
[+] score: 4
MiR-31 is an abundant miRNA in vascular smooth muscle cells, and its expression is significantly increased in proliferative smooth muscle cells and in vascular walls with neointimal growth [26]. [score:3]
Recent work shows that miR-31 controls smooth muscle phenotype and proliferation [26]. [score:1]
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18
[+] 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-17, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, hsa-mir-29a, hsa-mir-30a, hsa-mir-31, hsa-mir-32, hsa-mir-33a, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-106a, mmu-let-7g, mmu-let-7i, mmu-mir-27b, mmu-mir-30a, mmu-mir-30b, mmu-mir-126a, mmu-mir-9-2, mmu-mir-135a-1, mmu-mir-137, mmu-mir-140, mmu-mir-150, mmu-mir-155, mmu-mir-24-1, mmu-mir-193a, mmu-mir-194-1, mmu-mir-204, mmu-mir-205, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-143, mmu-mir-30e, hsa-mir-34a, hsa-mir-204, hsa-mir-205, hsa-mir-222, mmu-let-7d, mmu-mir-106a, mmu-mir-106b, hsa-let-7g, hsa-let-7i, hsa-mir-27b, hsa-mir-30b, hsa-mir-135a-1, hsa-mir-135a-2, hsa-mir-137, hsa-mir-140, hsa-mir-143, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-126, hsa-mir-150, hsa-mir-193a, hsa-mir-194-1, mmu-mir-19b-2, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-30d, mmu-mir-200a, 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-23a, mmu-mir-24-2, mmu-mir-29a, mmu-mir-31, mmu-mir-92a-2, mmu-mir-34a, rno-mir-322-1, mmu-mir-322, rno-let-7d, rno-mir-329, mmu-mir-329, rno-mir-140, rno-mir-350-1, mmu-mir-350, hsa-mir-200c, hsa-mir-155, mmu-mir-17, mmu-mir-25, mmu-mir-32, mmu-mir-200c, mmu-mir-33, mmu-mir-222, mmu-mir-135a-2, mmu-mir-19b-1, mmu-mir-92a-1, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-7b, hsa-mir-194-2, mmu-mir-194-2, hsa-mir-106b, hsa-mir-30c-1, hsa-mir-200a, hsa-mir-30e, hsa-mir-375, mmu-mir-375, mmu-mir-133b, hsa-mir-133b, 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-7b, rno-mir-9a-1, rno-mir-9a-3, rno-mir-9a-2, rno-mir-17-1, rno-mir-19b-1, rno-mir-19b-2, rno-mir-23a, rno-mir-24-1, rno-mir-24-2, rno-mir-25, rno-mir-27b, rno-mir-29a, 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-32, rno-mir-33, rno-mir-34a, rno-mir-92a-1, rno-mir-92a-2, rno-mir-106b, rno-mir-126a, rno-mir-135a, rno-mir-137, rno-mir-143, rno-mir-150, rno-mir-193a, rno-mir-194-1, rno-mir-194-2, rno-mir-200c, rno-mir-200a, rno-mir-204, rno-mir-205, rno-mir-222, hsa-mir-196b, mmu-mir-196b, rno-mir-196b-1, mmu-mir-410, hsa-mir-329-1, hsa-mir-329-2, mmu-mir-470, hsa-mir-410, hsa-mir-486-1, hsa-mir-499a, rno-mir-133b, mmu-mir-486a, hsa-mir-33b, rno-mir-499, mmu-mir-499, mmu-mir-467d, hsa-mir-891a, hsa-mir-892a, hsa-mir-890, hsa-mir-891b, hsa-mir-888, hsa-mir-892b, rno-mir-17-2, rno-mir-375, rno-mir-410, mmu-mir-486b, rno-mir-9b-3, rno-mir-9b-1, rno-mir-126b, rno-mir-9b-2, hsa-mir-499b, mmu-let-7j, mmu-mir-30f, mmu-let-7k, hsa-mir-486-2, mmu-mir-126b, rno-mir-155, rno-let-7g, rno-mir-15a, rno-mir-196b-2, rno-mir-322-2, rno-mir-350-2, rno-mir-486, mmu-mir-9b-2, mmu-mir-9b-1, mmu-mir-9b-3
Similarly, within the differentially expressed pool of miRNAs, 10 were identified that are intimately involved in regulating intracellular trafficking pathways, including: miR-7b-5p, miR-9-5p, miR-31-5p, miR-92a-3p, miR-106-5p, miR-126-3p, miR-150-5p, miR-204-5p, miR-222-3p, and miR-322-5p (S2 Fig). [score:4]
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[+] score: 4
Recent studies have identified that many miRs [11], such as miR-1, miR-21, miR-29, miR-31, miR-143/145, and miR-221/222, play important roles in neointimal hyperplasia by regulating the functions of VSMCs. [score:2]
A number of miRs, such as, miR-1, miR-21, miR-29, miR-31, miR-143/145 and miR-221/222, were verified to be involved in neointimal hyperplasia by regulating the functions of VSMCs [11]. [score:2]
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[+] score: 3
The total number of their target genes is between 114 (1st rank, “early” miR-495) and 45 (10th rank, “early” miR-31 and miR-133b) connections. [score:3]
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[+] score: 3
2) Some miRNAs, including let-7 family (let-a, -b and -c), miR-16, miR-23b, miR-26, miR-31 and miR-375, were always highly expressed either before or after transdifferentiation (data not shown). [score:3]
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[+] score: 3
Katsure et al[33] reported that miR-31 played an positive role in endothelial-mesenchyme transition (EndMT) involved in development and pathogenesis through integrating TGF-β and TNF-α signaling. [score:2]
Recent studies have found that miR-31 plays an important role in proliferation of vascular smooth muscle cells[32] and promotes the left ventricular remo deling of SHR. [score:1]
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[+] score: 3
One study has shown that serum miR-93, miR-146a, miR-31 are significantly upregulated in VD compared to controls (Dong et al., 2015). [score:3]
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[+] score: 3
In the discovery of Yamagishi et al., the Epi2miR pathway can be described as the regulatory process wherein under the control of EZH2 and SUZ12 (two important components of polycomb repressive complex), H3K9me and H3K27me histone modification regulates miR-31 and then affects NIK. [score:3]
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[+] score: 2
Several miRNAs, including miR-21 [11], miR-1, miR-206 [12], miR-31, and miR-499-5p [13] are reported to be dysregulated in myocardial infarction, suggesting a fundamental role in AMI. [score:2]
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[+] score: 2
In parallel an increase in the levels of miR-31, and miR-494 that were implicated in dystrophin and mitochondrial regulation and an increase in DNMT3a and DNMT3b proteins and global DNA methylation levels suggest that hHcy plays a causal role in enhanced fatigability through mitochondrial dysfunction which involves epigenetic changes. [score:2]
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[+] score: 2
The rno-miR-31 is the only miRNAs that has been previously reported in PKD [34]. [score:1]
We also chose rno-miR-31 as another candidate for qPCR due to its previous verification in PKD/Mhm (cy/+) rat mo del [34]. [score:1]
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[+] score: 1
Furthermore, eight miRNAs (mir-31, mir-122, mir-219-2-3p, etc. ) [score:1]
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