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37 publications mentioning hsa-mir-520b

Open access articles that are associated with the species Homo sapiens and mention the gene name mir-520b. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 97
We also found that the expression level of members of the two clusters, miR-520b and miR-302c, were negatively correlated with their targeted genes based on gene expression analysis We identified the expression patterns of miRNAs and gene transcripts in the undifferentiation of human embryonic stem cells; among the miRNAs that are highly expressed in undifferentiated embryonic stem cells, the miR-520 cluster may be closely involved in hES cell function and its relevance to chromatin structure warrants further study. [score:11]
To understand the predominant function of differentially expressed miRNA in the current study, we focused on miR-302c and miR-520b which were upregulated exclusively in hES and their correlation with computational predicted targeted genes. [score:8]
To infer the function of these miRNAs, we predicted 2,436 targets for the miR-302 cluster and 4,691 targets for the miR-520 cluster by querying the public database miRNAMap 2.0, and 2,284 target genes were shared by both clusters suggesting functional similarity. [score:7]
Our results confirmed the recent report that majority of miRNA genes in hES cells were expressed from Chromosomes 19 and X [55] and demonstrated the significant upregulation of miR-520 cluster in hES cells. [score:6]
Among the hES signature miRNAs, the miR-520 cluster shared a similar expression pattern and seed sequence as the well known miR-302 family and targeted the same genes as the miR-302 family. [score:5]
The mean of the correlation coefficients between the two sets, targeted and non -targeted genes, was significantly different (p = 0.0003 for miR-302c and p = 0.049 for miR-520b) (Figure 5). [score:5]
The distribution of correlation coefficients for miR-520b-target gene pairs (red line) was also shifted toward negative side compared to the miR-520b-non-target gene pairs (blue line) and the mean of correlation coefficients was significant (p = 0.049). [score:4]
Among the miRNAs upregulated in hES cells, we observed 7 miRNAs were located in the miR-302 cluster and 21 miRNAs were located in miR-520 cluster. [score:4]
The upregulation of miR-302 cluster and miR-520 cluster in hES cells suggests their ability to modulate local chromatin states which is necessary for stem cell pluripotency [58, 59]. [score:4]
In addition, we identified 12 other hES upregulated miRNAs in this cluster: miR-302a, miR-302b, miR-302c, miR-302d, miR-519b, miR-519c, miR-520a, miR-520b, miR-520c, miR-520d, miR-520e which share a consensus seed sequence: AAGUGC [24]. [score:4]
In addition, we identified 21 hES upregulated miRNAs that were co-localized in a cluster on chromosome 19, the miR-520 cluster, many of which shared consensus seed sequence with miR-302 family and which can be used as candidate biomarkers for pluripotency (Additional file 1). [score:4]
Along with the reports of miR-302 family on chromosome 4 [16, 17, 19, 25, 26], several groups have reported the expression of members of miR-520 cluster on chromosome 19 in hES cells [24, 26, 29]. [score:3]
The expression of miR-520b was 26-fold greater in hES cells then in EB cells (P < 0.05) and it was detected only in two types of adult cells HMVEC and HUVEC. [score:3]
The miR-302 cluster and miR-520 cluster target large groups of genes which share overlapping functions based on Gene Ontology (GO) analysis. [score:3]
Gene Ontology (GO) enrichment analysis confirmed that the inferred functions of miRNAs within the miR-302 and miR-520 clusters were overlapping based on their involvement in cell growth, negative regulation of cellular metabolic process, negative regulation of transcription, and small GTPase mediated signal transduction. [score:3]
This was also true for the miR-520b-target genes. [score:3]
Using qRT-PCR we found that the expression levels of miR-302b, miR-302c, miR-367, miR-200c, miR-519b, and miR-520b were much higher in hES cells than in either EB or adult cells (Figure 6, panel A). [score:3]
Especially, members of the miR-302 cluster on chromosome 4 and miR-520 cluster on chromosome 19 were highly expressed in undifferentiated hES cells. [score:3]
Expression of levels of miR-200c, miR-302b, miR-302c, miR-367, miR-519b, and miR-520b were the greatest in hES cells (panel A). [score:3]
To visualize the functions of these miRNA targeted genes, a binary (red indicate participate in the functional category and green indicate not) heatmap was used to indicate functional commonality among all miRNAs in miR-302 and miR-520 clusters. [score:3]
Figure 8 Sequence and GO analysis of the miR-302 cluster and miR-520 cluster. [score:1]
The members of the miR-302 and miR-520 clusters had similar sequences; they shared a consensus seed sequence: AAGUGC (panel A, seed sequence is highlighted by the purple rectangle). [score:1]
At the Gene Ontology level, miR-520b, miR-302b, miR-302c, miR-302d, miR-519c, miR-520a, and miR-302a formed a cluster (significant GO terms shown as red), and they shared GO terms related to chromatin structure modifications (Panel B). [score:1]
Less is known about the function of the miR-520 cluster. [score:1]
In particular, miR-302a, miR-302b, miR-302c, miR-302d, miR-519b, miR-519c, miR-520a, miR-520b, miR-520c, miR-520d, and miR-520e had a consensus seed sequence: AAGUGC (Figure 8, panel A). [score:1]
Besides these 9 miRNAs, we also identified 12 more miRNAs in this cluster; they were miR-515-5p, miR-517a, miR-517b, miR-517c, miR-519e, miR-520b, miR-520d, miR-520f, miR-520h, miR-521, miR-525-3p, and miR-526b*. [score:1]
Functional comparison of miR-302 cluster and miR-520 cluster. [score:1]
MiR-520b, miR-302b, miR-302c, miR-302d, miR-519c, miR-520a and miR-302a were clustered closely base on the 48 GO terms analyzed. [score:1]
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2
[+] score: 39
The ASA -mediated upregulation of miR-520b suppresses HBXIP expression and then blocks the HBXIP/HOXB13 axis, overcoming TAM resistance. [score:8]
The qRT-PCR assay revealed the negative association between the expression of HBXIP and miR-520b, where miR-520b showed higher expression levels in TAM-sensitive MCF-7 and T47D cells but lower expression levels in MCF-7-HBXIP and TAM-resistant BT474 cells (Additional file  4: Figure S6b). [score:6]
All siRNAs, the miR-520b inhibitor, and the control inhibitor were purchased from RiboBio Co. [score:5]
Moreover, introducing the miR-520b inhibitor into BT474 cells achieved an impressive blocking effect on the ASA -mediated suppression of the HBXIP/HOXB13 axis (Additional file  4: Figure S6c, d). [score:5]
Previously, our group reported that miR-520b could directly target HBXIP in breast cancer [29]. [score:4]
Previously, our group reported that miR-520b could directly target the 3′UTR of HBXIP mRNA [29]. [score:4]
Here, we uncovered that ASA could suppress HBXIP via inducing miR-520b, a tumor suppressor miRNA, but the regulation mechanism of miR-520b mediated by ASA needs more investigation in the future. [score:4]
Notably, ASA dose -dependently promoted the expression of miR-520b in BT474 cells (Additional file  4: Figure S6a). [score:3]
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3
[+] score: 32
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]
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]
Expression of the C19MC miRNAs in the iPSCs was generally two-fold or greater than that in the parental cell lines; the highest level of expression was 8.375 log [2](fold change) in miR-520b (Table  1). [score:5]
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]
However, the miR-520 and miR-302/372 families share a significant number of target genes (Fig.   3a) suggesting common biological functions. [score:3]
The results showed that 1185 putative shared genes were obtained between the miR-520 and -302/372 families (Fig.   3a, blue box and Additional file 1: Table S1), suggesting that the miR-520 subfamily might share similar biological functions with the miR-302/372 family. [score:1]
Hence, it is highly likely that the group I miR-520 miRNAs may also contribute to reprogramming, as supported by the predicted involvement of miR-520 miRNAs in the reprogramming-related apoptosis and cell proliferation pathways (see Fig.   4 and below). [score:1]
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4
[+] score: 24
The expression of eleven microRNAs (miR-10a, miR-21, miR-96, miR-135, miR-141, miR-182, miR-200b, miR-205, miR-429, miR-520b, miR-1244) formerly shown to be upregulated in urothelial bladder cancer were studied in corresponding normal and cancerous tissue samples of patients undergoing nephroureterectomy for UUTUC. [score:6]
We observed a significant overexpression of miR-21, miR-96, miR-135, miR-141, miR-182, miR-205, miR-429, miR-520b (all p<0.001) in UUTUC; the microRNAs miR-10a (p = 0.012) and miR-200b (p = 0.006) showed a distinct trend towards upregulation, whereas miR-1244 (p = 0.600) was similar in normal and malignant tissue. [score:6]
MicroRNA expression allowed differentiation of normal and cancerous tissue: miR-21, miR-96, miR-135, miR-141, miR-182, miR-205, miR-429 and miR-520b were significantly overexpressed. [score:5]
In order to investigate the role of microRNAs as non-invasive biomarkers in patients with UUTUC, the expression of eleven microRNAs (miR-10a, miR-21, miR-96, miR-135, miR-141, miR-182, miR-200b, miR-205, miR-429, miR-520b, miR-1244) earlier shown to be upregulated in urothelial cancer of the bladder [13– 20], was analyzed [11] in corresponding normal ureter and UUTUC tissue. [score:4]
Especially miR-21, miR-96, miR-135, miR-141, miR-182, miR-205, miR-429 and miR-520b were distinctly overexpressed in UUTUC. [score:3]
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5
[+] score: 11
Other miRNAs from this paper: hsa-let-7b, hsa-mir-15a, hsa-mir-19a, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-27a, hsa-mir-28, hsa-mir-30a, hsa-mir-100, hsa-mir-30c-2, hsa-mir-30d, hsa-mir-181a-2, hsa-mir-210, hsa-mir-181a-1, hsa-mir-221, hsa-mir-1-2, hsa-mir-15b, hsa-mir-30b, hsa-mir-122, hsa-mir-132, hsa-mir-141, hsa-mir-191, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125a, hsa-mir-195, hsa-mir-200c, hsa-mir-1-1, hsa-mir-30c-1, hsa-mir-34b, hsa-mir-34c, hsa-mir-30e, hsa-mir-371a, hsa-mir-372, hsa-mir-373, hsa-mir-375, hsa-mir-151a, hsa-mir-429, hsa-mir-449a, hsa-mir-483, hsa-mir-193b, hsa-mir-520e, hsa-mir-520f, hsa-mir-520a, hsa-mir-520c, hsa-mir-520d, hsa-mir-520g, hsa-mir-520h, hsa-mir-548a-1, hsa-mir-548b, hsa-mir-548a-2, hsa-mir-548a-3, hsa-mir-548c, hsa-mir-548d-1, hsa-mir-548d-2, hsa-mir-449b, hsa-mir-151b, hsa-mir-320b-1, hsa-mir-320b-2, hsa-mir-891a, hsa-mir-935, hsa-mir-1233-1, hsa-mir-548e, hsa-mir-548j, hsa-mir-548k, hsa-mir-548l, hsa-mir-548f-1, hsa-mir-548f-2, hsa-mir-548f-3, hsa-mir-548f-4, hsa-mir-548f-5, hsa-mir-548g, hsa-mir-548n, hsa-mir-548m, hsa-mir-548o, hsa-mir-548h-1, hsa-mir-548h-2, hsa-mir-548h-3, hsa-mir-548h-4, hsa-mir-1275, hsa-mir-548p, hsa-mir-548i-1, hsa-mir-548i-2, hsa-mir-548i-3, hsa-mir-548i-4, hsa-mir-1973, hsa-mir-548q, hsa-mir-548s, hsa-mir-548t, hsa-mir-548u, hsa-mir-548v, hsa-mir-548w, hsa-mir-548x, hsa-mir-1233-2, hsa-mir-548y, hsa-mir-548z, hsa-mir-548aa-1, hsa-mir-548aa-2, hsa-mir-548o-2, hsa-mir-548h-5, hsa-mir-548ab, hsa-mir-548ac, hsa-mir-548ad, hsa-mir-548ae-1, hsa-mir-548ae-2, hsa-mir-548ag-1, hsa-mir-548ag-2, hsa-mir-548ah, hsa-mir-548ai, hsa-mir-548aj-1, hsa-mir-548aj-2, hsa-mir-548x-2, hsa-mir-548ak, hsa-mir-548al, hsa-mir-548am, hsa-mir-548an, hsa-mir-371b, hsa-mir-548ao, hsa-mir-548ap, hsa-mir-548aq, hsa-mir-548ar, hsa-mir-548as, hsa-mir-548at, hsa-mir-548au, hsa-mir-548av, hsa-mir-548aw, hsa-mir-548ax, hsa-mir-548ay, hsa-mir-548az, hsa-mir-548ba, hsa-mir-548bb, hsa-mir-548bc
In patients with asthenozoospermia, two studies found that hsa-miR-27a [47, 56, 57], hsa-miR-548b-5p, hsa-miR-548c-5p and hsa-miR-548d-5p are up-regulated [47], while hsa-miR-34b-3p [47, 51], hsa-miR-520 h and hsa-miR-520d-3p are downregulated [47]. [score:7]
These miRNAs are expressed in spermatozoa and are involved in spermatogenesis (hsa-miR-34b-3p, hsa-miR-27a), embryonic development (hsa-miR-520 family) or in signaling pathways and human tumorigenesis (hsa-miR-548 family). [score:4]
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6
[+] score: 9
Keklikoglou and colleagues show that overexpression of miR-520/373 members reveals a strong downregulation of transforming growth factor-β (TGF- [β]) signaling and a negative correlation between miR-520c and TGFBR2 expression was observed in estrogen receptor negative (ER(-)) breast cancer patients[20]. [score:8]
The identification of stem cell specific miRNAs(miR-520, miR-302, miR-372, and miR-373) [40, 41], which was predicted to be increased on PAA is an indication that the PAA tissue environment may allow the PNET cells to return to a less differentiated state (S1 Dataset). [score:1]
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7
[+] score: 9
Conversely, mature miR-371, miR-520 and miR-302b (Figure 2B, C) appeared to be expressed in the stem cell populations only (hES and lt-NES), while their corresponding precursors were present both in stem cells and neuronal differentiating cultures. [score:3]
Intriguingly, the maintenance of precursor expression in neuronal cultures for the pluripotency -associated miR-371 and miR-520, as well as for miR-302 might indicate that these miRNAs have further functional roles beyond the switch from self-renewal to differentiation. [score:3]
Among the miRNAs expressed only in hES cells (Group 3), we found miR-371 and miR-520 (Figure 2C), which are known to be associated with pluripotency [29]– [31]. [score:3]
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8
[+] score: 9
The elucidation of the coordinated activity of miR-17-92 and miR-520 miRNAs, as well as of the regulatory networks that they are able to establish with their target genes, can largely contribute to i) the understanding of the physiology of hES cells development and differentiation and to ii) the exploitation of their potential as best candidate resources for both cell replacement therapy and development research. [score:6]
What is of more interest is that these biclusters group together miR-17-92 gene cluster members with those belonging to another important miRNA gene cluster, i. e. miR-520. [score:1]
The association of miR-17-92 with miR-520 was not detected either in mirDIP-A or in biclusters extracted from miRTarBase. [score:1]
Above all, HOCCLUS2 was able to group together, at high levels of the hierarchy, members of the miR-17-92 gene cluster with those belonging to the miR-520 gene cluster. [score:1]
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9
[+] score: 8
While we have not explored this possibility in the current manuscript, we note that even if such transcripts prevail in T-ALL cases, the most upstream canonical poly-adenylation site would only protect the MRE corresponding to miR-520-3p, miR-140-3p (both of which we showed to have no effect on reporter expression recovery upon mutagenesis assays) and the 4th MRE for miR-520-5p, which we showed that, together other two MREs for miR-520-5p, is not sufficient to recover the reporter expression. [score:4]
Interestingly, miR-101 [20, 43- 52], miR-140-5p [53- 56], miR-520-5p [57], and miR-485-5p [58- 60], are all reported as putative tumor suppressors in different cancers. [score:3]
The miRNAs miR-520-3p C. and miR-140-3p E. are not predicted to bind to TAL1 3′UTR, nevertheless the putative MRE were mutated as depicted. [score:1]
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10
[+] score: 8
Other miRNAs from this paper: hsa-mir-93, hsa-mir-34a, hsa-mir-34c, hsa-mir-519a-1, hsa-mir-519a-2
In particular, IFN-γ increased expression of miR-520b able to inhibit MICA transcript levels in different types of cancer cell lines (39). [score:5]
d. ↑ Cytotoxicity(25)(26) ER -induced stress CHOP↑ ULBP1↑ MULT1 Intestinal epithelial cells ↑ Cytotoxicity(27) Steady state STAT3 ↑ MICAColonrectal cancerMultiple myeloma↑ Cytotoxicity↑ IFNγ↑ Cytotoxicity(28)(29) Steady state IKZE1/3, IRF4 ↑ MICA Multiple myeloma ↑ Cytotoxicity(30, 31) RNA SPLICING Steady state RBM4 ↓ ULBP1 HAP1 cell line n. d. (32) POSTTRANSCRIPTIONAL Steady state AUF1 ↓ ULBP2, MICB Epithelial cells n. d. (33) Steady statemiR34a, cmiR-519a-3pmiR-93miR-20a↓ ULBP2↓ MICA, ULBP2↓ MICA, MICB, ULBP3↓ MICA, MICB, ULBP2Melanoma cell linesMammary epithelial cell lineGlioma cell linesCancer cell lines↓ Cytotoxicity↓ Cytotoxicity↓ Cytotoxicity↓ Cytotoxicity(34)(35)(36)(37, 38) IFNγ miR-520b ↓ MICA Cancer cell lines n. d. (39) HCMV, KSHV, and EBVmiR-UL112;miRK12-7; andmiR-BART2-5 ↓ MICB Infected HFF cells; cancer cell lines ↓ Cytotoxicity(40, 41) JCV miR-J1-3p ↓ ULBP3 Infected cancer cell lines ↓ Cytotoxicity(42) Posttranslational Steady state Ubiquitination ↓ MULT1 Cancer cell lines n. d. (43) KSHV K5 ubiquitin ligase ↓ MICA Cancer cell lines ↓ Cytotoxicity(44) Histamine Ubiquitination ↓ MICA Monocytic leukemia ↓ Cytotoxicity(45) Steady state ADAMs and MMPs (protease -mediated shedding) ↓ MICA, MICB, ULBP2 Cancer cell lines↓ Cytotoxicityn. [score:3]
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11
[+] score: 8
In previous study, Deepak et al. showed that miR-520b could inhibit MICA gene expression by binding on the promoter region and probably regulating transcription factors that important for MICA expression [17]. [score:8]
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12
[+] score: 7
Akin to the cell lines semi-quantitative revealed an upregulation of 3 miRNAs and again, as further example of that cluster, results were supplemented with qRT-PCR analyses for miR-520. [score:4]
We have shown that all thyroid adenomas with 19q13 rearrangements express significantly higher levels (p≤0.003133) of miR-520 than samples without 19q13 rearrangements (adenomas and surrounding thyroid tissue; for details see Table 1) (Figure 3b). [score:3]
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13
[+] score: 6
The existing literature implicated hsa-miR-520 h as an important target of ABCG2. [score:3]
Wang and colleagues observed that it resulted in inhibition of cell migration and invasion and decreasing rate of side population cells through transfection of hsa-miR-520 h into Panc-1 cells [30]. [score:3]
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14
[+] score: 6
miR-520 in hepatocellular carcinoma (HCC) cellsThe expression levels of miR-520e were decreased dramatically in HCC cells and clinical HCC tissues resulting from DNA hypermethylation in the upstream region of miR-520e locus, whereas silencing of the expression of miR-520e promoted cell proliferation [50]. [score:5]
miR-520 in hepatocellular carcinoma (HCC) cells. [score:1]
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15
[+] score: 6
Additionally, it was reported that hsa-miR-520 h downregulates ABCG2 in pancreatic cancer cells leading to inhibition of migration, invasion, and side population cells [19]. [score:6]
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16
[+] score: 5
Other miRNAs from this paper: hsa-mir-17, hsa-mir-20a, hsa-mir-195, hsa-mir-106b, hsa-mir-29c
Zhang W, et al. found that miR-520b is able to inhibit the growth of hepatoma cells by targeting MEKK2 or cyclin D1 both in vitro and in vivo [49]. [score:5]
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17
[+] score: 5
In addition, recent studies have reported that the miR-520 cluster, which is overexpressed in human ES cells, also acts as a tumor suppressor, and that introduction of miR-520h mimics into pancreatic cancer cells results in reduction of side population cells. [score:5]
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18
[+] score: 5
The authors used a siRNA against the EphA2 oncogene in a preclinical mo del of ovarian cancer and boosted the antitumour effects by addition of miR-520-3d, which synergistically inhibited the EphA2 expression in cancer cells. [score:5]
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19
[+] score: 5
In addition, several other miRNAs located on chromosome 19q13.42, such as miR-520g, miR-520h, and miR-520b, have been found to be downregulated in multiple myeloma [53]. [score:4]
We observed focal areas of hypomethylation of miR-520 and 5′ from the coding sequence in lymphomas, which may represent a permissive state for the binding of putative transcriptional repressors. [score:1]
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20
[+] score: 5
Importantly, miR-520-5p has previously been reported to inhibit expression of the EMT-related gene TWIST1 [38]. [score:5]
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21
[+] score: 4
The tumor suppressor p21, regulating transition through the cell cycle and acting downstream of p53, has already been associated with hsa-miR520 belonging to the miR-106/302 family [14]. [score:4]
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22
[+] score: 4
Indicated are select oncomiRs from the miR-17-92 and miR-106b-25 clusters and miR-520/373 family, which all have enriched putative target sites in Ago1-bound sequences. [score:3]
Interestingly, approximately one third of the 49 miRNAs are known oncomiRs including those from the miR-17-92 and miR-106b-25 clusters, as well as the miR-520/373 family (Figure 6B, Table S9). [score:1]
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23
[+] score: 4
The mir-520 group suppresses NFκB and TGF-β signaling, again in the context of cancerous cells [27], but given the roles of both signaling molecules in cytokine signaling and regulation, it is likely that this microRNA has alternative functions in these ILCs. [score:4]
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24
[+] score: 4
Other previously identified miRNAs are a chromosome 19 microRNA cluster (C19MC) including miR-517a, miR-519b, miR-520b, miR-520b, and miR-521, which were found to be highly expressed in human stem cells [10]; the miR-290 cluster was only detected at high levels in mouse stem cells [11]. [score:3]
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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25
[+] score: 4
Other miRNAs from this paper: hsa-mir-17, hsa-mir-93, hsa-mir-155
01493-07 17908789 8. Hu N. Zhang J. Cui W. Kong G. Zhang S. Yue L. Bai X. Zhang Z. Zhang W. Zhang X. miR-520b Regulates migration of breast cancer cells by targeting hepatitis B X-interacting protein and interleukin-8 J. Biol. [score:4]
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26
[+] score: 3
The ceRNA pair MEG3-MCL1 putatively shares 16 common miRNAs including miR-28, miR-181d, miR-520a, miR-520b and miR-876-3p and show comparable high co -expressions in breast and colon, especially in colon (MEG3 (66.2): MCL1 (37.9)). [score:3]
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27
[+] score: 3
The miRNA-520 cluster on chromosome 19 was highly expressed in undifferentiated hESCs, and might be closely involved in hESC function [156, 166]. [score:3]
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28
[+] score: 3
Then, we artificially altered the expression level of miR-520-3p by HOXA-AS2, si-HOXA-AS2, miR-520c-3p or antisense miR-520c-3p (Anti-520-3p) in breast cancer cells, and qRT-PCR was used to validate the transfection efficiency (P < 0.05, Figure 6C, 6D). [score:3]
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[+] score: 3
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-mir-16-1, hsa-mir-17, hsa-mir-18a, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-20a, hsa-mir-21, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-29a, hsa-mir-31, hsa-mir-99a, hsa-mir-100, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-106a, hsa-mir-16-2, hsa-mir-192, hsa-mir-199a-1, hsa-mir-208a, hsa-mir-30c-2, hsa-mir-147a, hsa-mir-10a, hsa-mir-34a, hsa-mir-181b-1, hsa-mir-199a-2, hsa-mir-203a, hsa-mir-204, hsa-mir-217, hsa-mir-219a-1, hsa-mir-221, hsa-mir-222, hsa-mir-223, hsa-mir-200b, hsa-mir-27b, hsa-mir-30b, hsa-mir-122, hsa-mir-125b-1, hsa-mir-132, hsa-mir-140, hsa-mir-142, hsa-mir-143, hsa-mir-145, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-126, hsa-mir-146a, hsa-mir-150, hsa-mir-185, hsa-mir-193a, hsa-mir-195, hsa-mir-200c, hsa-mir-155, hsa-mir-181b-2, hsa-mir-30c-1, hsa-mir-219a-2, hsa-mir-296, hsa-mir-130b, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-302d, hsa-mir-374a, hsa-mir-375, hsa-mir-378a, hsa-mir-330, hsa-mir-328, hsa-mir-342, hsa-mir-325, hsa-mir-424, hsa-mir-429, hsa-mir-450a-1, hsa-mir-486-1, hsa-mir-146b, hsa-mir-497, hsa-mir-520e, hsa-mir-520f, hsa-mir-520a, hsa-mir-520c, hsa-mir-520d, hsa-mir-520g, hsa-mir-520h, hsa-mir-450a-2, hsa-mir-503, hsa-mir-608, hsa-mir-625, hsa-mir-629, hsa-mir-663a, hsa-mir-1271, hsa-mir-769, hsa-mir-378d-2, hsa-mir-675, hsa-mir-147b, hsa-mir-374b, hsa-mir-663b, hsa-mir-378b, hsa-mir-378c, hsa-mir-374c, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-378f, hsa-mir-378g, hsa-mir-378h, hsa-mir-378i, hsa-mir-4661, hsa-mir-219b, hsa-mir-203b, hsa-mir-378j, hsa-mir-486-2
In HepG2 cells, EGCG differentially represses the expression of five miRNAs (miR-30b*, miR-453, miR-520-e, miR-629, and miR-608) involved in inflammatory pathways, the peroxisome proliferators-activated receptors (PPAR) signaling pathway, the insulin signaling pathway, glycolysis and gluconeogenesis, oxidative phosphorylation, and glutathione metabolism [127]. [score:3]
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Several miRNA families, including the human (hsa)-miR-302, hsa-miR-106, hsa-miR-372, hsa-miR-17, hsa-miR-520, hsa-miR-195 and hsa-miR-200 families [155] were up-regulated specifically in hPSCs compared to mature differentiated cell types. [score:3]
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Therefore, when we discuss the functions of miR-373 here, we should bear in mind that other members of miR-520/373 family may possess the same functions. [score:1]
miR-373 is one member of miR520/373 family, which consists of three different miRNA clusters possessing identical seed region, miR-302/367, miR-371/372/373 and miR-520 [8, 18, 22]. [score:1]
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miR-373 belongs to the miR-520/-373 family, which consists of three different miRNA clusters (miR-302/-367, miR-371/-372/-373, and miR-520) [27]. [score:1]
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miR-372, miR-373, miR-302, miR-520 and some other miRNAs are members of miR-93 family. [score:1]
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By comparison, miRNA transcripts of the C19MC cluster (miR-512, miR-516b, miR-520, and miR-525) were unchanged (Fig. 5). [score:1]
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We can see that, while bicluster Z' associates MUC17 with miR-17, miR-20a and miR-20b (Figure 9(a)), biclusters at levels 3 and 4 (Figures 9(b) and 9(c)) also include other miRNAs, some belonging to the miR-17-92 gene cluster and others to the miR-520 gene cluster. [score:1]
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Interestingly, except for isomiR of hsa-miR-520 g, other isomiRs with 3′ additions had the same 5′ ends and “seed sequences” with their canonical miRNA sequences in the miRBase database. [score:1]
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Thus, in breast cancer, which represents the most common malignancy among women in the world, miRNAs such as miR-9, miR-10b, miR-21, miR-103/107, miR-132, miR-373, and miR-520 stimulate metastasis, while miR-7, miR-30, miR-31, miR-126, miR-145, miR-146, miR-200, miR-205, miR-335, miR-661, and miRNAs of the let-7 families in contrast impair the different steps of metastatic process, from epithelial-to-mesenchymal transition to local invasion to colonisation and angiogenesis [61]. [score:1]
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