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36 publications mentioning hsa-mir-520f

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

1
[+] score: 289
Other miRNAs from this paper: hsa-mir-26a-1, hsa-mir-26b, hsa-mir-26a-2
Among the 32 up-regulated, 3 miRNAs were determined to be up-regulated by an infinite fold change at an extremely low expression level in the normal group and miR-520f ranked first among them. [score:9]
Three target genes prediction websites were performed to predict target genes and we found that FGF16 was one of the direct targets of miR-520f. [score:8]
In the current study, forced expression of FGF16 pheno-copied the effects of miR-520f over -expression in HCC cells, which sustaining a role of miR-520f in regulating FGF16 expression in HCC. [score:8]
Three target genes prediction websites (Targetscan, PicTar and miRDB) were applied to predict the potential targets of miR-520f. [score:7]
To future determine whether miR-520f down -expression resulted in the inhibition of HCC cells metastasis in vivo, the parental or miR-520f inhibitor transfected HCC cells were injected into mice via vein tail, and metastasis loci was determined five weeks later. [score:7]
As expected, up-regulation of FGF16 rescued miR-520f inhibitor -mediated growth and metastasis in HepG2 and PLC/PRF/5 cells (Figure 4D-4F). [score:6]
Down-regulation of FGF16 in miR-520f mimic transfected HCC cells inhibited colonies formation. [score:6]
In contrast to miR-520f over -expression, we found larger width in healing of miR-520f inhibitor transfected HCC cells (Figure 3G). [score:5]
The effect of miR-520f inhibitor on colony formation was reversed by over -expression of FGF16 in HepG2 and PLC/PRF/5 cells. [score:5]
FGF16 in HepG2 cells were inhibited after cells transfected with miR-520f inhibitor. [score:5]
Transwell invasion revealed over -expression of FGF16 significantly increased cells invasionupon transfection with miR-520f inhibitor. [score:5]
Short hairpin RNA (shRNA) targeting FGF16 (shFGF16), scrambled shRNA (shCTL), miR-520f/normal control (NC) mimic, and miR-520f/NC inhibitor were synthesized by GenePharma (Shanghai, China). [score:5]
As expected, inhibition effects on invasion were discovered in miR-520f inhibitor transfected HCC cells (Figure 3H). [score:5]
We found that down -expression of FGF16 effectively inhibited clone formation and metastasis in HCC cells that transfection with miR-520f (Figure 4A-4C). [score:5]
Wound healing revealed over -expression of FGF16 significantly increased cells migration upon transfection with miR-520f inhibitor. [score:5]
On the other hand, ectopically expression of FGF16 resulted in a markedly FGF16 levels increase in HCC cells that pre-transfection with miR-520f inhibitor. [score:5]
Down -expression of miR-520f in HCC cell resulted in the inhibitory effects growth and metastasis both in vitro and in vivo. [score:5]
To explore whether FGF16 reversed the roles of miR-520f in HCC cell aggressiveness, we manipulated the expression of FGF16 in HepG2 and PLC/PRF/5 cells that ectopic expression of miR-520f. [score:5]
The luciferase activities in the reporter containing the 3′-UTR of WT FGF16 was significantly suppressed, whereas miR-520f mimic had no obviously inhibition effect on the luciferase activities of reporter containing 3′-UTR of MUT FGF16 (Figure 2B and Supplementary Figure 1). [score:5]
Subsequently, we demonstrated that FGF16 over -expression strikingly restored cell growth, mobility and invasion phenotypes in HCC cells that pre -transfected with miR-520f inhibitor. [score:5]
Furthermore, miR-520f regulated HCC growth and metastasis partly via regulating FGF16, and altered the expression of FGF16 reversed the effect of miR-520f in HCC growth and metastasis. [score:5]
To further verify that miR-520f directly target 3′UTR of FGF16 gene, the interaction between the 3’UTR of FGF16 and miR-520f was validated by luciferase analysis. [score:4]
assays future demonstrated that FGF16 was markedly inhibited in HepG2 cells that transfected with miR-520f, and was elevated in HepG2 upon transfected with miR-520f inhibitor (Figure 2F and 2G). [score:4]
suggested the regulatory role of miR-520f down -expressing on proliferation index Ki67 in the tumor tissues (Figure 7E). [score:4]
Because miR-520f regulated the protein expression of FGF16, we next investigated whether FGF16 exert a direct regulation on the aggressiveness of HCC. [score:4]
miR-520f is up-regulated in HCC. [score:4]
Next, we verified whether the expression of FGF16 was regulated by miR-520f in HepG2 and PLC/PEF/5 cells. [score:4]
Herein, we identified miR-520f to be up-regulated in HCC cell lines and HCC tissues in our data. [score:4]
In this current study, we reported that miR-520f was remarkably up-regulated in HCC cells and clinical tissues, and was associated with the clinical prognosis of HCC. [score:4]
Knocked-down of FGF16 reversed the effects of miR-520f over -expression in HCC cell proliferation and aggressiveness. [score:4]
Transwell assay suggested that transfection of miR-520f inhibitor in HepG2 and PLC/PRF/5 inhibited cells invasion in vitro. [score:4]
The mRNA level of FGF16 in both HCC cells was significantly decreased after cells were transfected with miR-520f inhibitor. [score:3]
Conversely, inhibition of miR-520f significantly increased FGF16 levels in HepG2 and PLC/PRF/5 cells. [score:3]
In contrast, ectopic expression of miR-520f promoted the growth and metastasis ability of HCC cells. [score:3]
Overexpression of miR-520f promoted the growth and metastasis of HCC cells. [score:3]
The biological effects of miR-520f down -expression on HCC progression were also further examined using a xenograft tumor mo del. [score:3]
HepG2 and PLC/PRF/5 cells transfected with miR-520f inhibitor or control cells were implanted in nude mice. [score:3]
Overexpression of miR-520f decreased the mRNA level of endogenous FGF16 in both HepG2 and PLC/PRF/5 cells. [score:3]
As expected, the mice injected with miR-520f over -expressing cells possessed a greater degree of metastasis loci (Figure 7C). [score:3]
Schematic presentation of miR-520f target prediction by silico analyses. [score:3]
Wound healing revealed down -expression of FGF16 markedly decreased cells migration upon transfection with miR-520f mimic. [score:3]
Moreover, we found the positive relationship between miR-520f and FGF16 expression in HCC, which corroborated the biological relevance of miR-520f/FGF16 network in HCC. [score:3]
The expression of miR-520f was positively related to the level of FGF16. [score:3]
As shown in Figure 2E, the secreted FGF16 in medium were reduced in miR-520f over -expressing HepG2 and PLC/PEF/5 cells. [score:3]
Firstly, miR-520f over -expressing HCC cells were implanted subcutaneously into nude mice. [score:3]
To uncover the potential roles of miRNA -mediated growth, migration and invasion in HCC cells, HepG2 and PLC/PRF/5 were transfected with miR-520f or miR-520f inhibitor. [score:3]
As showed in Figure 7D, tumors formed by miR-520f down -expressing cells exhibited a smaller size and mass than tumors formed by the control cells. [score:3]
HepG2 and PLC/PRF/5 cells were transfected with miR-520f mimic, miR-520f inhibitor or shFGF16 utilized Lipofectamine [®] 2000 Transfection Reagent (Invitrogen). [score:3]
Subsequently, we utilized the xenograft mo del wherein the miR-520f over -expression HCC cells were injected via tail-vein. [score:3]
As shown in Figure 2C and 2D, the levels of FGF16 were assessed in HepG2 and PLC/PEF/5 cells that were transfected with miR-520f mimic or miR-520f inhibitor. [score:3]
Remarkably, miR-520f over -expressing HCC cells formed solid tumor mass in the inoculation site (Figure 7A). [score:3]
FGF16 is a target of miR-520f. [score:3]
Our findings imply that miR-520f plays pivotal oncogenic roles in HCC progression and hints its potential as a therapeutic target for HCC. [score:3]
Transwell invasion revealed down -expression of FGF16 markedly decreased cells invasion upon transfection with miR-520f mimic. [score:3]
Representative images of H&E-stained lung from mice injected with control cells or cells transfected with miR-520f inhibitor. [score:3]
Representative images of H&E-stained lung from mice injected with control cells or miR-520f over -expression cells. [score:3]
The expression of miR-520f in HCC cell lines and HCC tissues. [score:3]
In this study, we identified the over -expression of miR-520f in clinical HCC tissues and HCC cell lines. [score:3]
Histologic analysis revealed the number of metastatic lesions formed by miR-520f inhibitor cells was significantly reduced (Figure 7F). [score:3]
Colony assay revealed transfection of miR-520f inhibitor in HepG2 and PLC/PRF/5 cells reduce cellular growth in vitro. [score:2]
The HepG2 and PLC/PRF/5 cells transfected with miR-520f inhibitor showed lower growth and clone formation, as compared to control (Figure 3C and 3D). [score:2]
FGF16 is directly modulated by miR-520f. [score:2]
Transwell assay shown that miR-520f over -expression increased the invasion of HepG2 and PLC/PRF/5 in vitro. [score:2]
Immunohistochemical staining showed higher level of Ki67 in miR-520f over -expressing tumor tissues compared to the control tumor tissues (Figure 7B). [score:2]
tw/ym500v2/) revealed miR-520f is the most significantly up-expressed in HCC compared with normal. [score:2]
Wound-healing assay was performed to determine the effect of miR-520f inhibitor in HepG2 and PLC/PRF/5 cellular mobility in vitro. [score:2]
To investigate the mechanisms responsible of miR-520f for HCC growth and metastasis, bioinformatics analyses were performed to search for miR-520f targets. [score:1]
Colony formation analysis revealed transfection of miR-520f mimic in HepG2 and PLC/PRF/5 cells accelerate cellular progression. [score:1]
In human pancreatic cancer PANC-1 cells, miR-520f enhanced sensitivity to gemcitabine. [score:1]
Although miR-520f has not been linked to EMT or invasion before, it has been described to play a vital role in drug resistance [17, 18]. [score:1]
The effect of miR-520f on malignant progression of HCC cells in vivo. [score:1]
Altogether, these findings indicated that FGF16 was a core element which mediated miR-520f -induced pro-tumor effects in HCC. [score:1]
ELISA analysis of the secreted FGF16 levels in medium after HCC cells transfected with miR-520f mimic. [score:1]
Lastly, we examined the roles of miR-520f in HCC cells growth and dissemination in vivo by using nude mice mo dels of HCC. [score:1]
Conditioned medium collected from HCC cells transfected with miR-520f mimic or mimic-NC was subjected to ELISA. [score:1]
Taken together, these findings indicated that miR-520f contributed to HCC cells growth and metastatic in vivo. [score:1]
In Transwell analysis, miR-520f obviously accelerated the invasive of HCC cells (Figure 3F). [score:1]
qRT-PCR analysis was applied to determine the level of miR-520f in four HCC cell lines. [score:1]
Figure 7The effect of miR-520f on malignant progression of HCC cells in vivo (A). [score:1]
The level of miR-520f was detected by qRT-PCR in 58 cases of HCC tissues and 27 corresponding normal tissues. [score:1]
Survival analysis was conducted to assess the prognostic value of miR-520f in overall survival (OS) of patients with HCC. [score:1]
Furthermore, miR-520f increased the sensitivity of a cisplatin resistant neuroblastoma cell line to etoposide and cisplatin [19]. [score:1]
FGF16 reverses the effect of miR-520f -mediated HCC cell aggressiveness. [score:1]
Of relevance, we found that patients possess high level of miR-520f exhibited a poor overall survival (Figures 1C and Supplementary Table 2). [score:1]
The wide-type (WT) and mutant (MUT) 3′-UTR region of FGF16 were fused with luciferase reporter and co -transfected with miR-520f mimic or NC mimic into 293T cells. [score:1]
The miR-520f mimic with pmirGLO-FGF16 3′-UTR WT vector or pmirGLO-FGF16 3′-UTR MUT vector were co -transfected into 293T cells using Lipofectamine [®] 2000. [score:1]
All results suggested that miR-520f was positively associated with malignancy of HCC. [score:1]
Next, we explored the clinical outcomes of HCC patients with different level of miR-520f. [score:1]
In conclusion, our research identifies the potential mechanism underlying the pro-tumor growth and metastasis of miR-520f/FGF16 axis in HCC. [score:1]
These findings indicated miR-520f played a role in HCC cell growth, mobility and invasion in vitro. [score:1]
MiR-520f impairs aggressiveness of HCC cells in in vivoLastly, we examined the roles of miR-520f in HCC cells growth and dissemination in vivo by using nude mice mo dels of HCC. [score:1]
The level of miR-520f was assessed through mirVanaTM qRT-PCR microRNA Detection Kit (GeneCopoeia) and the mRNA of FGF16 was determined using SYBR Green quantitative Real-time PCR Master Mix kit in Biosystems 7300 Real-Time PCR system (ABI, Foster City, CA, USA). [score:1]
The mRNA level of FGF16 was remarkably increased when HepG2 and PLC/PRF/5 cells transfected with miR-520f mimic. [score:1]
In addition, analysis the level of miR-520f and FGF16 in HCC tissues exhibited a positively correlation (Figure 2H) and these results were consistent with HCC cell lines. [score:1]
Tumor growth kinetics (mean ± SD) of cells that transfected with miR-520f mimic versus control cells in nude mice. [score:1]
Finally, the similar results were also obtained in the four HCC cell lines, among which miR-520f level is higher in HCC cell lines than LO2 cells (Figure 1D). [score:1]
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2
[+] score: 61
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 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]
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 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 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]
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]
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]
Less is known about the function of the miR-520 cluster. [score:1]
Functional comparison of miR-302 cluster and miR-520 cluster. [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]
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3
[+] score: 31
MSC expression of the eight C19MC miRNAs could be grouped in three expression patterns: group A, which included miR-512-3p and -520c-3p, showed very low or undetectable expression in the MSCs; expression of the group B miR-520d-5p, 519b-3p and -524-5p was detected in at least one or both MSC cell lines, whereas miR-520f-3p, -517a-3p and -520g-3p in group C were all expressed all three MSC cell lines (Fig.   1b and Table  2). [score:11]
Despite en bloc and high-level C19MC expression in JEG-3 cells, only four of the eight miRNAs, namely miR-520d-5p of Group B as defined above for stem cell expression, and all three Group C miRNAs, miR-520f-3p, -517a-3p and -520g-3p, were shown to be expressed in the normal placenta cell line Hs799. [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]
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: 29
The downregulated levels of transcripts with the common seed-complementarities were low (P≤10 [−14]); however, those with own seed sequence-complementary sequence, AAGCACU, was high (P≤10 [−57]), indicating that the target recognition of miR-520f is slightly fluctuated. [score:6]
In the promoter analyses, miR-302a, miR-372, miR-373, miR-520c, and miR-520f duplexes showed the effects to increase the expression of proE-cad178-Luc and proE-cad670-Luc (Figure 6B, and D). [score:3]
of a one-sided K-S test for seed -dependent off-target effects is as follows: transcripts with complementary seed sequences of the opposite strand of dsEcad640, P = 0.999; those of miR-302a, P = 0.266; those of miR-372, P = 0.449; those of miR-373, P = 0.953; those of miR-520c, P = 0.031; those of miR-520f, P = 0.998. [score:3]
of a one-sided K-S test for seed -dependent off-target effects are as follows: transcripts with seed-complementary sequences of dsEcad640, P≤10 [−59]; those of miR-302a, P≤10 [−45]; those of miR-372, P≤10 [−20]; those of miR-373, P≤10 [−39]; those of miR-520c, P≤10 [−40]; those of miR-520f using common seed sequence, P≤10 [−14]; miR-520f using own seed sequence, P≤10 [−57]. [score:3]
To assess the parallel genome-wide regulation by dsEcad640 and the members of miR-302/372/373/520 family, microarray analyses were performed using PC-3 cells transfected with each of the miR-302a, miR-372, miR-373, miR-520c, and miR-520f duplexes, as well as with dsEcad640 at 24 hour. [score:2]
The opposite strand miRNAs of miR-372 and miR-520f are not annotated. [score:1]
The seed sequence of dsEcad640 antisense strand (AAGUGCU) is same as those of the miR-302/372/373/520 miRNA family members, miR-302a, miR-372, miR-373, miR-520a-3p, and miR-520f, although the seed sequence of miR-520f is shifted by 1 nt to 1–7 nt from 2–8 nt (Figure 1B). [score:1]
The transcripts of ZEB1, MED8, MTPN, LATS2, and RAB31 possess seed-complementarities to either of dsEcad640, miR-302a, miR-372, miR-373, miR-520c, and miR-520f. [score:1]
Chemically synthesized dsEcad640, miR-302a, miR-372, miR-373, miR-520c, and miR-520f duplexes were transfected into PC-3 cells. [score:1]
The effects of dsEcad215, dsEcad302, dsEcad640, miR-302a, miR-372, miR-373, miR-520c, miR-520f, and siZEB1_CDS were determined using stably transfected cells with each luciferase reporter, and shown as Renilla/firefly. [score:1]
The microarray profile of miR-520f showed relatively low correlation coefficients with the other miRNAs ranging from 0.34 to 0.41, although its correlation coefficient with dsEcad640 was 0.55 (Figure 7). [score:1]
Then, the effects on ZEB1 CDS were determined by the transfection of miR-302a, miR-372, miR-373, miR-520c, and miR-520f duplexes along with pLuc-CDS and pGL3-Control into PC-3 cells (Figure 1). [score:1]
The silencing activities by dsEcad640, miR-302a, miR-372, miR-373, miR-520c, and miR-520f on wild-type pLuc-CDS (WT), pLuc-CDS-m640-1, -2, and -1+2 are shown as Renilla/firefly. [score:1]
Microarray profiles of transcripts containing common seed-complementary sequences of dsEcad640 and members of miR-302/372/373/520 family by the transfection of (A) dsEcad640, (B) miR-302a duplex, (C) miR-372 duplex, (D) miR-373 duplex, (E) miR-520c duplex, and (F) miR-520f duplex. [score:1]
Microarray profiles of transcripts containing variable seed-complementary sequences of the opposite strands in their 3′UTRs by the transfection of (A) dsEcad640, (B) miR-302a duplex, (C) miR-372 duplex, (D) miR-373 duplex, (E) miR-520c duplex, and (F) miR-520f duplex. [score:1]
MiR-302a, miR-372, miR-373, miR-520c, miR-520f miRNA duplexes were synthesized to form the same sequences and structures described in miRBase [51]. [score:1]
The seed sequences of dsEcad640 sense strand, miR-302*, the opposite strand of miR-372, miR-373*, miR-520c-5p, and the opposite strand of miR-520f, are different (Figure 1B). [score:1]
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5
[+] score: 11
Among the miRNAs, the function of fifteen downregulated miRNAs (miR-1587, miR-4505, miR-1915-3p, miR-4466, miR-3162-5p, miR-4484, miR-5001-5p, miR-3940-5p, miR-4687-3p, miR-6068, miR-548ao-3p, miR-4687-5p, miR-1273g-3p, miR-877-3p, miR-4312) and the function of two miRNAs that were upregulated (miR-520f-3p, miR-4307) remain unknown. [score:7]
According to our findings, whereas the expression of five miRNAs (miR-369-5p, miR-586, miR-520f-3p, miR-4307 and 505-3p) were decreased, the expression of thirty-seven miRNAs increased in both the chronic and active group compared with the control group. [score:4]
[1 to 20 of 2 sentences]
6
[+] 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-520a, hsa-mir-520b, 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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7
[+] 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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8
[+] 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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9
[+] 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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10
[+] 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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11
[+] score: 7
The miRNA signatures generated for ER status (miR-342, miR-299, miR-217, miR-190, miR-135b, miR-218), for PR status (miR-520g, miR-377, miR-527-518a, miR-520f-520c) and for HER2/ neu status (miR-520d, miR-181c, miR-302c, miR-376b, miR-30e) include miRNAs that have previously been identified as dysregulated in breast cancer and other cancers [7, 9, 37- 43] and involved in the regulation of cell functions such as growth, apoptosis, migration and invasion [38, 42, 43]. [score:3]
Notably, two chromosomal locations account for a number of the dysregulated miRNAs in these predictive sets: Ch19q13 (miR-520g, miR-520d, miR-527-528a, miR-520f-520c, miR-181c) and Ch14q32 (miR-342, miR-299, miR-377, miR-376b). [score:2]
Stepwise ANN analysis identified predictive miRNA signatures corresponding with oestrogen (miR-342, miR-299, miR-217, miR-190, miR-135b, miR-218), progesterone (miR-520g, miR-377, miR-527-518a, miR-520f-520c) and HER2/ neu (miR-520d, miR-181c, miR-302c, miR-376b, miR-30e) receptor status. [score:1]
Similarly, four miRNA transcripts (miR-520g, miR-377, miR-527-518a, miR-520f-520c) were identified that predicted tumour PR status with 100% accuracy, and HER2/ neu status was predicted with 100% accuracy by a signature of five miRNAs (miR-520d, miR-181c, miR-302c, miR-376b, miR-30e) (Table 3). [score:1]
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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: 6
Figure 2 Table 3 MiRNAs Confirmation Ranks hsa-mir-507 dbDEMC2.0 1 hsa-mir-30e dbDEMC2.0 2 hsa-mir-9-2 dbDEMC2.0;Mir2desease 3 hsa-mir-520f dbDEMC2.0 4 hsa-mir-132 dbDEMC2.0 5 hsa-mir-424 dbDEMC2.0 6 hsa-mir-431 dbDEMC2.0 7 hsa-mir-34b dbDEMC2.0 8 hsa-mir-149 dbDEMC2.0 9 hsa-mir-185 dbDEMC2.0 10 Inputs: RDnet, denoted as G (V, E, W); specific disease d. Outputs: Top ranked d-related miRNA candidates. [score:3]
Figure 2 Table 3 MiRNAs Confirmation Ranks hsa-mir-507 dbDEMC2.0 1 hsa-mir-30e dbDEMC2.0 2 hsa-mir-9-2 dbDEMC2.0;Mir2desease 3 hsa-mir-520f dbDEMC2.0 4 hsa-mir-132 dbDEMC2.0 5 hsa-mir-424 dbDEMC2.0 6 hsa-mir-431 dbDEMC2.0 7 hsa-mir-34b dbDEMC2.0 8 hsa-mir-149 dbDEMC2.0 9 hsa-mir-185 dbDEMC2.0 10 Inputs: RDnet, denoted as G (V, E, W); specific disease d. Outputs: Top ranked d-related miRNA candidates. [score:3]
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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
Importantly, miR-520-5p has previously been reported to inhibit expression of the EMT-related gene TWIST1 [38]. [score:5]
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20
[+] 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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21
[+] 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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22
[+] 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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23
[+] 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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24
[+] 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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25
[+] 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-520a, hsa-mir-520b, 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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[+] score: 3
In particular, hsa-mir-520e, hsa-mir-518c-5p, and all six miRNA precursors were, resultingly, downmodulated in the high risk group, while hsa-mir-329-3p, hsa-mir-302d-3p, hsa-mir-520f, hsa-mir-511-5p, hsa-mir-509-3p, hsa-mir-519a-3p, hsa-mir-521, hsa-mir-520h, and hsa-mir-499a-5p were overexpressed. [score:3]
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27
[+] score: 3
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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28
[+] score: 2
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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[+] score: 1
Other miRNAs from this paper: hsa-mir-208a
For instance, rs7744 in 3′-UTR of MYD88 and rs696 in 3′-UTR of NFKBIA genes could disrupt the binding of miR-520f-3p and miR-208a-3p, respectively. [score:1]
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30
[+] score: 1
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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31
[+] score: 1
miR-372, miR-373, miR-302, miR-520 and some other miRNAs are members of miR-93 family. [score:1]
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32
[+] score: 1
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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[+] score: 1
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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[+] score: 1
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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[+] score: 1
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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36
[+] score: 1
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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