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42 publications mentioning hsa-mir-519d

Open access articles that are associated with the species Homo sapiens and mention the gene name mir-519d. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 144
Other miRNAs from this paper: hsa-mir-21
By using miRNA target prediction (DIANA-mT, miRanda, miRDB, and Targetscan), we proved MMP-2 and MMP-3 most probable miR-519d targets; transfection of miR-519d -mimic strongly inhibited CTGF -induced MMP-2 and MMP-3 expression. [score:11]
Furthermore, MEK or ERK inhibitors and mutants reversed CTGF -inhibited miR-519d expression (Fig. 4F), indicating that CTGF increases MMPs and migration as well as suppresses miR-519d through MEK/ERK pathway. [score:9]
We confirmed miR-519d expression using qRT-PCR, the miR-519d was down-regulated in MG-63/CTGF cells, and up-regulated in U-2 OS/CTGF-shRNA cells (Fig. 2A). [score:9]
MMP-2 and MMP-3 are the downstream target genes in CTGF-regulated miR-519dTo identify the mechanism of miR-519d-involved osteosarcoma migration, we searched for possible downstream genes using bioinformative screening analysis of miRNA target databanks: DIANA-mT, miRanda, miRDB, and Targetscan. [score:8]
CTGF increases MMP-2/-3 expression and promotes metastasis by down -regulating miR-519d through MEK and ERK pathways; CTGF inhibition presents a new therapeutic target. [score:8]
High CTGF expression was significantly associated with clinical stage and metastasis (Table 1); higher CTGF and lower miR-519d expression were linked with MMP-2 and MMP-3 expression, correlating with osteosarcoma development and metastasis. [score:8]
Our study screened 576 miRNAs from miRNome microRNA Profilers QuantiMir™ kit and found miR-519d most down-regulated in response to CTGF overexpression; miR-519d reportedly suppresses tumor formation in human hepatocellular carcinoma, making it an attractive candidate biomarker for prediction of anticancer treatment response [51, 52]. [score:8]
Among the significantly regulated miRNAs, miR-519d was the most down-regulated in response to CTGF overexpression (Supplementary Table 1). [score:7]
Results indicated CTGF inducing upregulation of MMP-2 and MMP-3 expression in human osteosarcoma cells by down -regulating miR-519d through MEK and ERK pathway and contributing the tumor metastasis. [score:7]
To further verify the direct effect of miR-519d on cell motility, we transiently transfected the miR-519d mimic or inhibitor into osteosarcoma cells, and found miR-519d mimic but not inhibitor blocked the CTGF -induced cell migration (Fig. 2C). [score:6]
From these four databanks overlapping between the predicted targets of miR-519d, the MMP-2 and MMP-3 were ranked as the most probable targets. [score:5]
To identify the mechanism of miR-519d-involved osteosarcoma migration, we searched for possible downstream genes using bioinformative screening analysis of miRNA target databanks: DIANA-mT, miRanda, miRDB, and Targetscan. [score:5]
CTGF increases cell migration by suppressing miR-519d expression. [score:5]
We indicated miR-519d directly repressing MMP-2 and MMP-3 protein expression through binding to 3'UTR of human MMP-2 and MMP-3 genes, thus negatively regulating MMP-2 and MMP-3 -mediated metastasis. [score:5]
In addition, directly applied CTGF in MG-63 cells and U-2 OS cells for 24 h reduced miR-519d expression in a concentration -dependent manner (Fig. 2B). [score:4]
The results show that CTGF increases MMPs expression and subsequently promotes tumor metastasis in human osteosarcoma by down -regulating miR-519d through MEK and ERK pathway. [score:4]
CTGF increases MMP-2 and MMP-3 expression and cell migration by down -regulating miR-519d. [score:4]
Taken together, these data demonstrated that miR-519d directly represses the MMP-2 and MMP-3 protein expression through binding to the 3'UTR of the human MMP-2 and MMP-3 gene. [score:4]
MMP-2 and MMP-3 are the downstream target genes in CTGF-regulated miR-519d. [score:4]
MEK/ERK pathway is involved in CTGF-induce migration and suppression of miRNA-519d. [score:3]
MEK/ERK pathway is involved in CTGF -mediated migration and suppression of miRNA-519d. [score:3]
Furthermore, transfection with miR-519d mimic abolished CTGF -induced MMP-2 and MMP-3 expression (Fig. 3E). [score:3]
Figure 2(A) The miR-519d expression in indicated cells was examined by qRT-PCR. [score:3]
MiR-519d mimic and inhibitor were purchased from Invitrogen (Carlsbad, CA). [score:2]
Taken together, CTGF increases osteosarcoma migration through down -regulating miR-519d. [score:2]
To examine whether miR-519d regulates the 3'UTR of MMP-2 and MMP-3, we constructed luciferase reporter vectors harboring the wild-type 3'UTR of the MMP-2 and MMP-3 mRNA (wt-MMP-2-3'UTR and wt-MMP-3-3'UTR) and vector containing mismatches in the predicted miR-519d binding site (mt-MMP-2-3'UTR and mt-MMP-3-3'UTR; Supplementary Fig. S1) and transfected these vectors into MG-63/CTGF and control cells. [score:2]
Repression of miR-519d by CTGF is critical in CTGF -mediated migration. [score:1]
Quantitative RT-PCR analysis of CTGF, MMP2, MMP-3, and miR-519d performed in osteosarcoma and normal samples, showed negative correlation between CTGF and miR-519d; positive correlation between CTGF and MMP-2, CTGF and MMP-3 (Fig. 6B-D). [score:1]
Clinical importance of CTGF, MMPs and miR-519d in osteosarcoma. [score:1]
Confirming significance of CTGF, MMPs, and miR-519d in clinical samples. [score:1]
In this study, transfection of cells with miR-519d mimic reduced CTGF -induced cell migration, meaning miR-519d can be an anti-metastatic gene. [score:1]
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2
[+] score: 108
To further examine whether the AMPK/p38 signaling pathway is involved in resistin-reduced miR-519d expression, we pre -treated cells with AMPK and p38 inhibitors or transfected them with AMPK and p38 siRNA, which was found to rescue resistin -inhibited miR-519d expression (Fig. 3F&G). [score:9]
Our results indicated that resistin induced up-regulation of MMP-2 expression and tumor metastasis by down-regulation of miR-519d through the AMPK/p38 pathway. [score:9]
In this study, whether miR-519d play a role in resistin -mediated metastasis was examined and found that resistin promotes tumor metastasis and MMP-2 expression by down-regulation of miR-519d expression through the AMPK/p38 signaling pathway in human chondrosarcoma. [score:8]
Taken together, high expressions of resistin and MMP-2, as well as reduced expression of miR-519d, were found to be associated with chondrosarcoma development and metastasis. [score:6]
Taken together, these data indicate that resistin promotes cell migration and MMP-2 expression by down-regulation of miR-519d through the AMPK/p38 signaling pathway. [score:6]
The JJ012 cells were pre -treated with AMPK and p38 inhibitors for 30 min or pre -transfected with specific siRNAs for 24 h followed by stimulation with resistin (3 ng/ml) for 24 h; and the (F, G) miR-519d expression and (H) MMP-2 3′ UTR activity were examined. [score:5]
As shown in Fig. 3E, resistin increased luciferase activity in the WT-MMP-2-3′ UTR plasmid but not in the MUT-MMP-2-3′ UTR, indicating that miR-519d directly represses MMP-2 protein expression via binding to the 3′ UTR of human MMP-2. Figure 3(A) The JJ012 and SW1353 cells were transfected with miR-519d mimic or inhibitor for 24 h, and cell migration ability was examined by Transwell assay. [score:5]
To further confirm resistin -mediated cell migration, MMP-2, and miR-519d expression in vivo, JJ012 cells stably expressing resistin shRNA were established. [score:5]
Following resistin treatment, we found that the miR-519d mimic but not the inhibitor abolished resistin -induced cell migration and MMP-2 expression (Fig. 3A and B). [score:5]
MiR-519d has been considered as an onco-miRNA in tumor progression, which could up-regulated by p53 and DNA hypo-methylation and then target to CDKN1A/p21, PTEN, AKT3 and TIMP2 [28]. [score:5]
To determine whether miR-519d was indeed involved in resistin -mediated cell migration and MMP-2 expression, an miR-519d mimic or inhibitor was transfected into chondrosarcoma cells. [score:5]
By overlapping the results of the DIANA-mT, miRanda, miRDB, and Targetscan databases, we found that MMP-2 was predicted to be a putative target of miR-519d. [score:5]
As shown in Fig. 3E, resistin increased luciferase activity in the WT-MMP-2-3′ UTR plasmid but not in the MUT-MMP-2-3′ UTR, indicating that miR-519d directly represses MMP-2 protein expression via binding to the 3′ UTR of human MMP-2. Figure 3(A) The JJ012 and SW1353 cells were transfected with miR-519d mimic or inhibitor for 24 h, and cell migration ability was examined by Transwell assay. [score:5]
Resistin appears to promote cell migration and MMP-2 expression through inhibition of miR-519d via the AMPK/p38 signaling pathway. [score:5]
Furthermore, we also found that the migration ability and MMP-2 expression were dramatically decreased, and that the miR-519d expression was increased in JJ012/Resistin-shRNA cells (Fig. 4B-D). [score:5]
Thus, resistin appears to suppress miR-519d expression through the AMPK/p38 pathway. [score:5]
By using RT-qPCR, we moreover found that resistin directly reduced miR-519d expression in a concentration -dependent manner (Fig. 3C). [score:4]
To demonstrate whether miR-519d specifically targeted the MMP-2 3′ UTR, we constructed luciferase reporter vectors harboring wild-type 3′ UTR of the MMP-2 mRNA (WT-MMP-2-3′ UTR) and mismatches in the predicted miR-519d binding site (MUT-MMP-2-3′ UTR; Fig. 3D). [score:3]
MiR-519d mimic and inhibitor were purchased from Invitrogen (Carlsbad, CA). [score:2]
MiR-519d is an important factor in resistin -induced cell migration and MMP-2 expression. [score:2]
In addition, miR-519d regulating MMP -dependent migration and metastasis is documented [29]. [score:2]
Correlations between (D) resistin/MMP-2, (E) resistin/miR-519d, and (F) MMP-2/mi-519d in human chondrosarcoma tissues. [score:1]
RT-qPCR analysis of resistin, MMP-2, and miR-519d performed in chondrosarcoma and normal samples showed a positive correlation between resistin and MMP-2; and negative correlations between resistin and miR-519d, MMP-2 and miR-519d (Fig. 5D-F). [score:1]
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3
[+] score: 82
Cluster 1 denotes miR-519d-regulated exclusive targets and the exclusive co-expressed proteins of these targets. [score:8]
Some of miR-21 targets are also the co-expressed proteins of miR-519d and other miRNA targets. [score:7]
That is, some of miR-519d targets are the co-expressed proteins of miR-21 and other miRNA targets. [score:7]
The sub-network that miR-519d and miR-21 jointly regulates is visualized in Fig. 6. We found that miR-519d and miR-21 share the same target PTEN and they also have their own exclusive targets. [score:6]
MiR-519d specifically regulates hepatocellular carcinoma and it is one of the miRNAs which have most targets among miRNAs regulating only one cancer. [score:5]
The three proteins are all co-expressed proteins of TIMP2 (degree = 22, betweenness centrality = 0.0308) that is one of miR-519d targets. [score:5]
It can be found that miR-519d also have targets with high degrees and betweenness centralities such as CDKN1A (degree = 253, betweenness centrality = 0.3611) and shared one target PTEN (degree = 92, betweenness centrality = 0.1124) with miR-21. [score:5]
Cluster 3 denotes the shared co-expressed proteins of exclusive targets for miR-519d and miR-21 respectively. [score:5]
The eclipse nodes in small size are co-expressed proteins of those targets of miR-519d and miR-21. [score:5]
Moreover, the specific targets of miR-519d and miR-21 also have common and exclusive co-expressed proteins respectively. [score:5]
Among these eclipse nodes, the orange nodes are targets of other miRNAs except miR-519d and miR-21, and the blue nodes are non-targets. [score:5]
To concretely explain the similarities and differences between miRNAs specifically regulating only one cancer and miRNAs generally regulating various cancers in our work, we extracted miR-519d and miR-21-regulated CePPIN for further analysis. [score:4]
The red circle nodes are direct targets of miR-519d and miR-21 respectively. [score:4]
Finally, we extracted miR-519d and miR-21-regulated CePPINs as an example to further testify our analysis and findings. [score:2]
MiR-519d only regulates hepatocellular carcinoma and miR-21 is involved in 12 cancers including hepatocellular carcinoma. [score:2]
Therefore, we can conclude that miR-519d may induce hepatocellular carcinoma through a regulation of proteasome, but the exact mechanism still need to be revealed in future researches. [score:2]
The visualization of miR-519d and miR-21-regulated CePPIN. [score:2]
The miR-21 and miR-519d-regulated CePPIN. [score:2]
The green diamond nodes are two miRNAs, namely miR-519d and miR-21. [score:1]
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4
[+] score: 56
miR-519, a microRNA that suppresses tumorigenesis and lowers expression of RNA -binding protein HuR, was upregulated in senescent cells. [score:8]
In conjunction with the finding that miR-519 reduced tumorigenesis in a xenograft mo del [32], we propose that the coordinated action of senescence -upregulated microRNAs can suppress tumor growth by reducing the levels of oncogenes or tumor promoters. [score:6]
Among the microRNAs showing increasing abundance with senescence, miR-519 was of particular interest because it was shown to inhibit translation of HuR and to diminish tumor growth [31, 32]. [score:5]
miR-519 was recently found to inhibit translation of the RNA -binding protein HuR through its interaction with the HuR coding region [31]. [score:5]
As indicated above, miR-519 was found to suppress tumor growth [32]. [score:3]
Overexpression of miR-519 induced senescence in WI-38 and HeLa cells. [score:3]
As shown here for miR-519, we postulate that these changes help to meet the needs of senescent cells in eliciting tumor suppression and growth arrest. [score:3]
Since HuR potently enhances the expression of cancer-promoting proteins, and reducing HuR levels promotes HDF senescence [11, 38], we propose that miR-519 represses tumor growth at least in part, by lowering HuR and thereby promoting senescence (Figs. 4 and 5). [score:3]
Additionally, miR-519 could further repress tumor growth by lowering the expression of other genes, such as ABCG2 or HIF-1α [46, 47]. [score:3]
In a separate study, miR-519 suppressed the growth of tumor xenografts in an HuR -dependent manner [32]. [score:3]
Accordingly, we postulate that one of the mechanisms by which miR-519 suppress tumor growth is by inducing senescence, and further propose that miR-519 triggers senescence -at least in part- by reducing HuR levels. [score:3]
Given that HuR promotes cell proliferation and decreases senescence [33, 34], we hypothesized that the elevated miR-519 in senescent cells (Figure 4A) might lower HuR expression in WI-38 HDFs, and hence promote senescence. [score:3]
We were particularly interested in the miR-519 family. [score:1]
Together, these data indicate that miR-519 reduced HeLa cell proliferation and promoted HeLa cell senescence. [score:1]
miR-519 -induced senescence in HDFs. [score:1]
miR-519 -induced senescence in HeLa cells. [score:1]
We previously reported that miR-519 represses the production of HuR, an RNA -binding protein which is highly abundant in cancer cells and is low in untransformed cells [11, 38]. [score:1]
Moreover, while HuR levels are high in tumors and low in normal tissues, miR-519 levels are high in normal tissues and low in cancer tissues [32]. [score:1]
Influence of miR-519 on the senescent phenotype of HeLa cells. [score:1]
Influence of miR-519 on WI-38 senescence. [score:1]
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5
[+] score: 51
As a result of the specific DNA binding, miR-519d is up-regulated by p53, whereas ERα mediates both down- and up-regulated expression of miR-515-5p induced by estrogens and tamoxifen, respectively. [score:9]
The numerical in brackets shows the ranking of each pathway Table 3 Common validated target genes shared between the C19MC-AAGUGC-miRNAs and the miR-302/-372 families AAGUGC-miRNASeed position [a] Target transcript miR-302/-372 C19MC miR-302c miR-520e I NIK[10, 15] miR-373 miR-520c I MT1-MMP, mTOR, SIRT1[14, 21] miR-372, -373 miR-520c, -520e I RelA[12] miR-302b, -372, -373 miR-520c, -520e I TGFβR2[9, 12] miR-520b, -520e I CD46[16] miR-302c miR-520c I MICA, MICB, ULBP2[17] miR-519a I RBL2[13] miR-512 IIa miR-519d, -520g IIb SMAD7[19, 20] miR-520g, -520h IIb DAPK2[18, 22] miR-302d, -372 miR-520b, -519b-3p, -520a-3p I CDKN1A[5, 6] miR-519e IIa miR-519d, -520h IIb [a]Group I seed position is the canonical nts 2-7; IIa is nts 1-6 and IIb is other non-canonical position, as defined in Fig.   2a The 2058 putative target genes were further subjected to GO analysis and KEGG pathway annotation (Fig.   3b-d). [score:7]
The numerical in brackets shows the ranking of each pathway Table 3 Common validated target genes shared between the C19MC-AAGUGC-miRNAs and the miR-302/-372 families AAGUGC-miRNASeed position [a] Target transcript miR-302/-372 C19MC miR-302c miR-520e I NIK[10, 15] miR-373 miR-520c I MT1-MMP, mTOR, SIRT1[14, 21] miR-372, -373 miR-520c, -520e I RelA[12] miR-302b, -372, -373 miR-520c, -520e I TGFβR2[9, 12] miR-520b, -520e I CD46[16] miR-302c miR-520c I MICA, MICB, ULBP2[17] miR-519a I RBL2[13] miR-512 IIa miR-519d, -520g IIb SMAD7[19, 20] miR-520g, -520h IIb DAPK2[18, 22] miR-302d, -372 miR-520b, -519b-3p, -520a-3p I CDKN1A[5, 6] miR-519e IIa miR-519d, -520h IIb [a]Group I seed position is the canonical nts 2-7; IIa is nts 1-6 and IIb is other non-canonical position, as defined in Fig.   2a The 2058 putative target genes were further subjected to GO analysis and KEGG pathway annotation (Fig.   3b-d). [score:7]
Activation of the C19MC miR-519d was shown to target CDKN1A/p21, PTEN, AKT3 and TIMP2, and is closely associated with the pathogenesis of hepatocellular carcinoma by promoting cell proliferation and invasion, and in inhibiting apoptosis [47]. [score:5]
However, construction of a Venn diagram showed that only 262 putative target genes are common between the miR-519 and miR-520 subfamilies in group I, indicating that the miR-519 and -520 subfamilies target different sets of genes. [score:5]
Transcription factors acting in trans are essential regulators of C19MC miRNA expression as shown by direct binding of p53 and the estrogen receptor α (ERα) to presumptive promoters of C19MC miR-519d and miR-515-5p, respectively, in chromatin immunoprecipitation assays [47, 48]. [score:4]
Genes targeted by either or both the miR-519 or -520 subfamilies are shown in different color boxes. [score:3]
Furthermore, one of the characteristics of target prediction, the sequence context surrounding the seed binding site of the target transcript [1], between the miR-519 and -520 subfamilies are also dissimilar (Fig.   2a). [score:3]
The group I miR-519 subfamily also shares 262 putative target genes with the miR-302/-372 families, far fewer than the miR-520 subfamily (Fig.   3a, red box). [score:3]
In this study, the putative target sets of the miR-519 and -520 subfamilies are overlapping gene sets predicted by two different prediction algorithms. [score:3]
The group I miRNAs are composed of the miR-519 and -520 subfamilies. [score:1]
Furthermore, it is noted that the AAGUGC seed position at 5’ end is variable among the C19MC-AAGUGC-miRNAs: subgroup I miRNAs, which includes eight miR-519 and -520 subfamilies, have the seed sequence located at the canonical and optimal 5’-nucleotide positions (nts) 2-7, as in the miR-302/-372 families; the seed sequence of the four subgroup IIa miRNAs is at location nts 1-6, and that of the remaining subgroup IIb miRNAs is at nts 3-8 and 4-9 (Fig.   2a). [score:1]
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6
[+] score: 25
However, the identification of target genes specific for miR-519d is especially challenging because it shares target sequence specificity with miR-17-5p, miR-20 A and B, as well as miR-106 A and B. Other microRNAs overexpressed more than twofold in human male breast cancer, but not yet described in female breast cancer are miR-183, miR-197, miR-493-5p, and 519d. [score:7]
miR-21, miR519d, miR-183, miR-197, and miR-493-5p were identified as most prominently up-regulated, miR-145 and miR-497 as most prominently down-regulated in male breast cancer. [score:7]
A recent publication describes the kallikrein family of serine proteases as potential targets of miR-519d, the second most prominently up-regulated microRNA in male breast cancer [22]. [score:6]
Up-regulation of miR-519d, miR-183, miR197, and miR-493-5p (more than twofold in comparison to gynecomastia, see Table 2) has not been reported so far in female breast cancer. [score:4]
Welch -based t-test demonstrates a statistically significant difference between carcinoma samples and the controls for miR-21, miR-145, and miR-497, but only a trend for miR-519d (Figure 3). [score:1]
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7
[+] score: 18
In hepatocellular carcinoma miR-519d is up-regulated by p53 and DNA hypomethylation and targets CDKN1A/p21, PTEN, AKT3 and TIMP2. [score:6]
Upregulation of miR-519d, which is observed in approximately 50% of HCCs, is positively associated with CpG island hypomethylation and wild-type p53 (Fornari et al., 2012). [score:4]
Recently, Fornari et al. (2012) reported that miR-519d is upregulated due to DNA hypomethylation in hepatocellular carcinoma (HCC). [score:4]
miR-519d is thought to act as an oncogenic miRNA (oncomir) through its targeting of p21, PTEN, AKT3, and TIMP2. [score:3]
miR-519d belongs to the chromosome 19 miRNA cluster (C19MC), which is the largest miRNA cluster in the human genome. [score:1]
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8
[+] score: 17
The mechanism underlying selective upregulation of the ORAI1 subunit is not known, but the post-transcriptional expression of the ORAI1 gene has been shown to be regulated by miR-519 using TargetScan/complementarity studies in HELA cells (Ab delmohsen et al., 2012). [score:9]
Whether similar regulation by MIR-519 occurs in hVF-HF is not known, but in our studies we were unable to detect MIR-519 expression in fibroblasts from non-failing or failing hearts, which is suggestive that other possible regulatory mechanisms are involved (Sauc et al., 2015). [score:5]
Growth inhibition by miR-519 via multiple p21-inducing pathways. [score:3]
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9
[+] score: 10
miR-517a/b, miR-517c, and miR-519d could suppress trophoblast cell migration and invasion by targeting a number of migration-related transcripts including CXCL6, FOXL2, NR4A2, and by upregulating the expression of sFlt-1 (7– 9). [score:10]
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10
[+] score: 9
Further, their data identified miR-519d down-regulation via connective tissue growth factor (CTGF) signaling as a pathway osteosarcoma cells utilize to upregulate MMP-3 and MMP-2 expression [17]. [score:9]
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11
[+] score: 9
In abdominal tissue, hsa-miR-520c-3p/520f, hsa-miR-519d and hsa-miR-183 were found to be associated with their target mRNAs, as well as being tissue differentially expressed. [score:5]
Seven of the miRNAs that were differentially expressed in both studies, have previously been reported to play a role in tissue development, obesity, T2D and metabolic disturbances (hsa-miR-34a [23], [32], hsa-miR-28-5p [32], hsa-miR-27b [13], [15], hsa-miR-326 [21], hsa-miR-204 [22], [23], hsa-miR-195 [32], hsa-miR-519d [29]). [score:4]
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12
[+] score: 9
An experiment on MKI67 indicated that the cellular growth of hepatocellular carcinoma can be suppressed by targeting MKI67 through miR-519d [81]. [score:5]
Hou Y. Cao W. Li L. Li S. Liu T. Wan H. Liu M. Li X. Tang H. MicroRNA-519d targets MKi67 and suppresses cell growth in the hepatocellular carcinoma cell line QGY-7703Cancer Lett. [score:4]
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13
[+] score: 8
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-17, hsa-mir-18a, hsa-mir-19a, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-20a, hsa-mir-21, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-27a, hsa-mir-29a, hsa-mir-30a, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-93, hsa-mir-100, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-107, mmu-let-7g, mmu-let-7i, mmu-mir-1a-1, mmu-mir-23b, mmu-mir-27b, mmu-mir-29b-1, mmu-mir-30a, mmu-mir-30b, mmu-mir-125a, mmu-mir-9-2, mmu-mir-133a-1, mmu-mir-136, mmu-mir-138-2, mmu-mir-181a-2, mmu-mir-24-1, mmu-mir-191, hsa-mir-196a-1, hsa-mir-148a, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-122, mmu-mir-143, mmu-mir-30e, hsa-mir-34a, hsa-mir-181a-2, hsa-mir-196a-2, hsa-mir-181a-1, mmu-mir-296, mmu-mir-298, mmu-mir-34c, mmu-let-7d, mmu-mir-130b, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-23b, hsa-mir-27b, hsa-mir-30b, hsa-mir-122, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-138-2, hsa-mir-143, hsa-mir-191, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125a, hsa-mir-136, hsa-mir-138-1, mmu-mir-19b-2, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-30d, mmu-mir-148a, mmu-mir-196a-1, mmu-mir-196a-2, 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-18a, mmu-mir-20a, mmu-mir-21a, mmu-mir-24-2, mmu-mir-29a, mmu-mir-29c, mmu-mir-27a, mmu-mir-92a-2, mmu-mir-93, mmu-mir-34a, mmu-mir-103-1, mmu-mir-103-2, mmu-mir-330, mmu-mir-346, hsa-mir-1-1, mmu-mir-1a-2, mmu-mir-107, mmu-mir-17, mmu-mir-19a, mmu-mir-100, mmu-mir-181a-1, mmu-mir-29b-2, mmu-mir-19b-1, mmu-mir-92a-1, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-138-1, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-34c, hsa-mir-296, hsa-mir-130b, hsa-mir-30e, hsa-mir-375, hsa-mir-381, mmu-mir-375, mmu-mir-381, hsa-mir-330, mmu-mir-133a-2, hsa-mir-346, hsa-mir-196b, mmu-mir-196b, hsa-mir-18b, hsa-mir-20b, hsa-mir-146b, hsa-mir-501, hsa-mir-503, mmu-mir-20b, mmu-mir-503, hsa-mir-92b, mmu-mir-146b, mmu-mir-669c, mmu-mir-501, mmu-mir-718, mmu-mir-18b, mmu-mir-92b, hsa-mir-298, mmu-mir-1b, hsa-mir-103b-1, hsa-mir-103b-2, hsa-mir-718, mmu-mir-21b, mmu-let-7j, mmu-mir-21c, mmu-mir-30f, mmu-let-7k, mmu-mir-9b-2, mmu-mir-9b-1, mmu-mir-9b-3
Several miRNAs are upregulated in adipose tissue in animal mo dels of metabolic disease and/or obesity, e. g. mir-125a [31], mir29 [32], and mir-143 [33], while adipose tissue miR-519d expression is associated with human obesity [15]. [score:8]
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14
[+] score: 8
It was reported that resistin promotes chondrosarcoma metastasis and MMP2 expression through activation of AMPK/p38 signaling pathway and down-regulation of miR-519d expression in mouse mo dels 64. [score:8]
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15
[+] score: 8
In human subcutaneous adipose tissue overexpression of miR-519d was reported to be associated with severe obesity [9]. [score:3]
No previous studies have reported miR-519d is differentially expressed in obesity or during adipogenic differentiation (Table 1). [score:3]
Adipocytes adipogenesis biomarkers microRNAs miR-27 miR-519d obesity. [score:1]
During adipogenesis miR-519d is stimulated in a dose -dependent manner, which suggests miR-519d may be a factor in adipocyte hypertrophy and increased adipose tissue mass in human obesity [9]. [score:1]
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[+] score: 7
Similarly, Hromadnikova et al. [17] detected a downregulation of 6 miRNAs (miR-517-5p, miR-518f-5p, miR-519a, miR-519d, miR-520a-5p, and miR-525) in placental tissues of 36 FGR pregnancies: compared to the previous studies, these results seem more robust since that authors investigated more types of miRNAs and used those that were previously demonstrated to be exclusively expressed or highly expressed in placental tissues. [score:5]
The significantly decreased expression of miR-519d, but not of miR-520a-5p and miR-525, was also confirmed by others on a larger cohort (50 healthy pregnancies compared with 45 FGR cases) [15]. [score:2]
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17
[+] score: 7
Mir-519 and -519E were also upregulated in cKit+ ILCs; these microRNAs have been shown to inhibit cell growth and thus promote cell survival [25]whereas mir-423 promotes cell growth by regulating the G(1)/S transition in the cell cycle in hepatocellular carcinoma cell lines [26]. [score:7]
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18
[+] score: 6
CAN-10-0145 20501828 6. Fornari F In hepatocellular carcinoma miR-519d is up-regulated by p53 and DNA hypomethylation and targets CDKN1A/p21, PTEN, AKT3 and TIMP2J. [score:6]
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[+] score: 6
PPAR-α has been shown to be the target of the up-regulated miR-519d in large artery stroke (Supplementary Data Table 2; [34]). [score:6]
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20
[+] score: 6
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-16-1, hsa-mir-17, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-20a, hsa-mir-21, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-29a, hsa-mir-30a, hsa-mir-98, hsa-mir-101-1, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-106a, hsa-mir-16-2, hsa-mir-192, hsa-mir-148a, hsa-mir-30c-2, hsa-mir-30d, hsa-mir-7-1, hsa-mir-7-2, hsa-mir-7-3, hsa-mir-10a, hsa-mir-10b, hsa-mir-34a, hsa-mir-210, hsa-mir-215, hsa-mir-200b, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-30b, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-125b-1, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-137, hsa-mir-138-2, hsa-mir-143, hsa-mir-144, hsa-mir-145, hsa-mir-152, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-126, hsa-mir-127, hsa-mir-138-1, hsa-mir-146a, hsa-mir-193a, hsa-mir-194-1, hsa-mir-206, hsa-mir-320a, hsa-mir-200c, hsa-mir-1-1, hsa-mir-155, hsa-mir-194-2, hsa-mir-106b, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-200a, hsa-mir-302a, hsa-mir-101-2, hsa-mir-34b, hsa-mir-34c, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-302b, hsa-mir-302c, hsa-mir-302d, hsa-mir-369, hsa-mir-371a, hsa-mir-340, hsa-mir-335, hsa-mir-133b, hsa-mir-146b, hsa-mir-519e, hsa-mir-519c, hsa-mir-519b, hsa-mir-519a-1, hsa-mir-519a-2, hsa-mir-499a, hsa-mir-504, hsa-mir-421, hsa-mir-320b-1, hsa-mir-320c-1, hsa-mir-320b-2, hsa-mir-190b, hsa-mir-301b, hsa-mir-302e, hsa-mir-302f, hsa-mir-320d-1, hsa-mir-320c-2, hsa-mir-320d-2, hsa-mir-320e, hsa-mir-371b, hsa-mir-499b
Small RNA regulation of some of the splicing control proteins has previously been reported; for example, the ELAV transcript, which encodes the HuR protein, a major modulator of mRNA stability and translation in addition to mRNA splicing [58], is subject to regulation by miRNAs miR-519, miR-16 and miR-125a in a variety of cell types including cervical, ovarian and colon cancer cell lines [59, 60, 61]. [score:5]
Ab delmohsen K. Srikantan S. Kuwano Y. Gorospe M. miR-519 reduces cell proliferation by lowering RNA -binding protein HuR levels Proc. [score:1]
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21
[+] score: 6
For example, hsa-miR-519d showed two different dominant sequences in normal and diseased samples, and they were inconsistent with canonical hsa-miR-519d. [score:3]
Except for hsa-miR-519d, fold changes always were less than 2, which suggested several abundant isomiRs with similar expression levels from a given miRNA locus (Table S4). [score:3]
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22
[+] score: 5
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-18a, hsa-mir-22, hsa-mir-29a, hsa-mir-30a, hsa-mir-93, hsa-mir-100, hsa-mir-29b-1, hsa-mir-29b-2, mmu-let-7g, mmu-let-7i, mmu-mir-1a-1, mmu-mir-29b-1, mmu-mir-30a, mmu-mir-30b, mmu-mir-124-3, mmu-mir-126a, mmu-mir-9-2, mmu-mir-133a-1, mmu-mir-146a, mmu-mir-200b, mmu-mir-203, mmu-mir-204, mmu-mir-205, hsa-mir-148a, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-30e, hsa-mir-10a, hsa-mir-34a, hsa-mir-203a, hsa-mir-204, hsa-mir-205, hsa-mir-218-1, hsa-mir-218-2, hsa-mir-221, hsa-mir-222, hsa-mir-200b, mmu-mir-34c, mmu-mir-34b, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-30b, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-126, hsa-mir-146a, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-30d, mmu-mir-148a, 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-18a, mmu-mir-22, mmu-mir-29a, mmu-mir-29c, mmu-mir-93, mmu-mir-34a, hsa-mir-200c, hsa-mir-1-1, mmu-mir-1a-2, mmu-mir-10a, mmu-mir-100, mmu-mir-200c, mmu-mir-218-1, mmu-mir-218-2, mmu-mir-221, mmu-mir-222, mmu-mir-29b-2, mmu-mir-124-1, mmu-mir-124-2, mmu-mir-9-1, mmu-mir-9-3, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-200a, hsa-mir-34b, hsa-mir-34c, hsa-mir-30e, hsa-mir-375, mmu-mir-375, hsa-mir-335, mmu-mir-335, mmu-mir-133a-2, hsa-mir-424, hsa-mir-193b, hsa-mir-512-1, hsa-mir-512-2, hsa-mir-515-1, hsa-mir-515-2, hsa-mir-518f, hsa-mir-518b, hsa-mir-517a, hsa-mir-516b-2, hsa-mir-516b-1, hsa-mir-517c, hsa-mir-519a-1, hsa-mir-516a-1, hsa-mir-516a-2, hsa-mir-519a-2, hsa-mir-503, mmu-mir-503, hsa-mir-642a, mmu-mir-190b, mmu-mir-193b, hsa-mir-190b, mmu-mir-1b, hsa-mir-203b, mmu-let-7j, mmu-mir-30f, mmu-let-7k, mmu-mir-126b, mmu-mir-9b-2, mmu-mir-124b, mmu-mir-9b-1, mmu-mir-9b-3
Significant expression of miRNAs within this cluster (miR-512-3p, miR-512-5p, mir-515-5p, miR-516b, miR-517a, miR-517c, miR-518b, miR-518f, miR-519a and miR-519d) was observed in the MaSC/basal population (Fig.   3b), whereas no highly expressed luminal-specific primate miRNAs were identified. [score:5]
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23
[+] score: 4
miR-519d could promote melanoma progression by downregulating EphA4 [31], among other mechanisms. [score:4]
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24
[+] score: 4
E) Quantification of SMYD2 protein level in HEK293T transfected with either pre-miR-519-3p or random miRNA sequences. [score:1]
D) Quantification of Smyd2 mRNA level in HEK293T transfected a plasmid containing either pre-miR-519-3p or random miRNA sequences. [score:1]
F) Western-blot of HEK293T protein extract, transfected either with pre-miR-519-3p or random miRNA sequences. [score:1]
Validation of Smyd2 mRNA interaction with miR-519. [score:1]
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25
[+] score: 4
Recently identified miRNAs, such as miR-9, miR-34a, miR-16, miR-125a, miR-29a, miR-200c, and miR-519, play crucial roles in regulating HuR expression through interaction of miRNAs with specific sites in the 3′UTR and 5′UTR of the HuR mRNA. [score:4]
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[+] score: 4
Furthermore, as predicted by Cytoscape_V2_8_3, hsa_circ_0036877 may function as a ceRNA to bind to miR-519d-3p and miR-15b-5p, thus affecting gene expression (Additional file  1: Figure S3D). [score:3]
Bars represent standard errors Previous studies show that miRNAs (miR-210 [24], miR-181a [25], miR-126-3p and miR-126-5p [26], miR-223 [27], miR-515 [28], and miR-519d [29]) are involved in the pathogenesis of PE. [score:1]
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[+] score: 4
MiR-519 represses the production of HuR, an RNA -binding protein very abundantly found in tumor cells and less expressed in untransformed cells, while the overexpression of HuR delays the senescent phenotype (83). [score:4]
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28
[+] score: 3
Interestingly, a recent study demonstrates that expression levels of seven placenta-specific miRNAs (miR-518b, miR-1323, miR-516b, miR-515-5p, miR-520h, miR-519d, and miR-526b) were significantly reduced in placentas from IUGR pregnancies than in placentas from uncomplicated pregnancies [146]. [score:3]
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29
[+] score: 3
Moreover, some miRNAs (miR-130, miR-27a/b, miR-378 and miR-519d) can directly regulate the levels of two critical transcription factors, peroxisome proliferator-activated receptor γ (PPARγ) and cytidine-cytidine-adenosine-adenosine-thymidine (CCAAT) enhancer binding protein α (C/EBPα), thus affecting the dynamics of adipogenesis (8– 11). [score:3]
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[+] score: 3
For example, miR-144, miR-937, miR-376, miR-519, and miR-548A-3P are shown to regulate a number of mRNAs, and HCK, NFKBIE, IL6, SHMT2, and MCM4 are regulated by several miRNAs. [score:3]
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31
[+] score: 3
Other miRNAs from this paper: hsa-mir-522
It may be miR-522 is dysregulated in the obese and thus contributes to the dysregulation of adipogenic pathways as suggested for another C19MC member, miR-519d [37]. [score:3]
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32
[+] score: 3
Our analysis shows a possible involvement of several members of the miR-515 family (such as miR-515-5p, miR-519 and miR-520a-3p/b/c-3p/d-3p/e/g/h), located at 19q13.4, in POF, since they are predicted to target FMR1 and FOXL2, two genes which are associated to POF [47], [48]. [score:3]
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33
[+] score: 2
Strongest regulation was observed for miR-519d, miR-512-3p and miR-1293 (Fig. 3C). [score:2]
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34
[+] score: 2
CDKN1A could be regulated by several miRNAs in many cancers, including miR-519d, miR-375, miR-31 and miR-663 [33– 35]. [score:2]
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35
[+] score: 2
Gene Name Protein Name Consensus Results CASP9 Caspase-9 hsa-miR-124 hsa-miR-182 hsa-miR-504 hsa-miR-506 hsa-miR-96 RIPK2 Receptor-interacting serine/threonine-protein kinase 2 hsa-miR-200b hsa-miR-200c GRB2 Growth factor receptor-bound protein 2 hsa-miR-182 CDK2 Cyclin -dependent kinase 2 hsa-miR-200b hsa-miR-200c hsa-miR-429 CASP8 Caspase-8 hsa-miR-17 hsa-miR-20b hsa-miR-495 hsa-miR-519d hsa-miR-93 RAF1 Rapidly Accelerated Fibrosarcoma (RAF) proto-oncogene serine/threonine-protein kinase hsa-miR-15a hsa-miR-15b hsa-miR-16 hsa-miR-195 hsa-miR-424 hsa-miR-497 With the development of systems biology, carcinogenesis could be interpreted as the malfunction of perturbed protein functional interaction networks in a cell, and therefore, analyses of apoptosis-related network from a systems-level perspective is of great significance [29, 30, 31]. [score:2]
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36
[+] score: 2
Additional miRNAs have also been found to regulate adipogenesis in human preadipocytes or stem cells, with miR-143 and miR-519d being proadipogenic and miR-130 and miR-138 being antiadipogenic. [score:2]
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37
[+] score: 2
In particular, the following miRNAs can regulate metastatic ability in osteosarcoma: miR-507 [38], miR-497 [39], miR-519d [23], miR-185 [40], miR-218 [40] and miR-200b [41]. [score:2]
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38
[+] score: 1
The miR-659-3p cluster also included miR-219-3p and miR-519-5p (Fig.   1b), which had less significant or no association with PFS (p = 0.036 and p = 0.12, respectively). [score:1]
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39
[+] score: 1
Serum miR-323-3p concentrations determined by real-time PCR were significantly elevated in EP and revealed more promising results than miR-517a, miR-519d, and miR-525-3p, with a 37% sensitivity rate (at a fixed-specificity of 90%) when used as a single marker. [score:1]
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40
[+] score: 1
Seed sequence examination indicated no similarities to the known seed sequences of pluripotency-specific miRNAs such as AAGUGC in miR-302b-3p, miR-373, miR-520e, miR-519c-3p, miR-520a-3p, and miR-520b; AGUGCC in miR-515-3p and miR-519e; and AAGUG in miR-519d. [score:1]
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41
[+] score: 1
Except miR-519d and -28-5p, all the other 11 miRNAs belonged to the 14 miRNA cluster. [score:1]
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42
[+] score: 1
2010.00683. x 20649821 8. Ab delmohsen K. Srikantan S. Kuwano Y. Gorospe M. miR-519 reduces cell proliferation by lowering RNA -binding protein HuR levels Proc. [score:1]
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