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18 publications mentioning hsa-mir-507

Open access articles that are associated with the species Homo sapiens and mention the gene name mir-507. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 319
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-mir-214, hsa-mir-15b
To verify whether miR-507 plays an important role in the migration and invasion through its target gene, Flt-1, we introduced the synthesized miR-507 mimics into MDA-MB-231 cells and miR-507 inhibitors into MCF-7. Stable miR-507 over -expression in MDA-MB-231 cells (MDA231/miR-507) and stable miR-507 down-regulation in MCF-7 cells (anti-miR507/MCF-7) were obtained. [score:10]
In summary, we showed that Flt-1 promoted the migration and chemotexis of breast-cancer cells by binding to PlGF-1. More remarkably, our findings suggest a novel role for miR-507 in inhibiting Flt-1 expression and in suppressing the migration and invasion of breast cancer by inhibiting PlGF-1 -induced actin polymerization. [score:9]
Expression of miR-507 in lower metastasis cell lines MCF-7 was set as evaluation criteria, high expression of miR-507 meant that the expression was higher than the criteria level, low expression of miR-507 meant that the expression was lower than the standard or equal the criteria level. [score:9]
These results suggest that 3′-UTR of Flt-1 is a direct target of miR-507, and miR-507 can directly regulate Flt-1 expression in breast-cancer cells. [score:8]
To conform if Flt-1 expression could be regulated by miR-507, we analyzed the expression of Flt-1 protein through the Western blot 48 h after being transfected by miR-507 mimic (miR-507), miR-507 inhibitor (ant-miR-507) in the MDA-MB-231, and MCF-7 cell lines, respectively. [score:8]
A previous study reported that the administration of miR-507 was effective in inhibiting the growth of tumors formed from A549 cells in nude mice by targeting NF-E2–related factor 2 (NRF2) as well as ME1, a known transcriptional target of NRF2 [18]. [score:7]
Mutation of miR-507 target sites of Flt-1 made the luciferase activity restore control cells (NC) level (Figure 2C), confirming that 3′-UTR of Flt-1 is a direct target of miR-507. [score:7]
Simultaneously, the expression of Flt-1 protein in tumor xenograft was down-regulated in mice injected with MDA231/miR507 cells (Figure 4C). [score:6]
In the current study, we reported that the expression of miR-507 was significantly down-regulated in invasive ductal carcinoma tissues and is inversely correlated with the tumor differentiation, lymphatic metastasis, and distant metastasis. [score:6]
PlGF-1 promoted migration and invasion of breast-cancer cells, and Flt-1 was required for cell migration and invasion mediated by PlGF-1. MiR-507 directly targets Flt-1. MiR-507 directly targets Flt-1, and. [score:6]
Considering the role of Flt-1 in breast cancer, our results suggested that miR-507 could suppress breast-cancer invasion by directly targeting the 3′-UTRs of the Flt-1 genes. [score:6]
Clinical information of the samples is described in detail in Table 1. For the experimental metastasis mouse xenograft mo del, MDA-MB-231 cells stably expressing miR-507 NC (MDA231/NC), miR-507 mimic lentiviral vector (MDA231/miR507), knocked-down Flt-1 expression (SiFlt-1/MDA231), the negative control (Scr/MDA231) were injected into their mammary fat pads of five-week-old female BALB/C-nu/nu nude mice (N = 10). [score:6]
Moreover, 5-aza-dC (DNA methyltransferase inhibitor) can increase miR-507 expression in breast-cancer cell lines and can reduce the invasive ability of breast-cancer cells. [score:5]
Our results also showed that miR-507 inhibited the PlGF-1 -induced actin polymerization by mediating Flt-1. Taken together, our results suggested that miR-507 functioned upstream of LIMK/cofilin and directly regulated PlGF-1 -induced actin polymerization. [score:5]
Overexpression of miR-507 inhibited the invasion of MDA-MB-231, consistent with the effect of silencing Flt-1 (Figure 2D). [score:5]
The result showed that tumors with a low level of miR-507 tended to express high levels of Flt-1, whereas tumors with a high level of miR-507 tended to express low levels of Flt-1 (Figure 5B). [score:5]
Down-regulation of miR-507 promoted the invasion of MCF-7, consistent with the effect of up -regulating Flt-1 (Figure 2E). [score:5]
Overexpression of miR-507 in breast-cancer cells inhibits invasion. [score:5]
To examine whether miR-507 targets Flt-1 mRNA though its predicted pairing sites, we cloned the 3′-UTR of Flt-1 containing miR-507 targets into a luciferase construct. [score:5]
Hence, miR-507 appeared to negatively regulate tumor invasion and metastasis in breast-cancer patients by targeting Flt-1. Figure 5, and the function of miR-507 A. expression of miR-507 in 30 pairs of frozen invasive ductal carcinoma tissues (T) compared with their corresponding adjacent non-cancerous tissues (ANT). [score:5]
The results showed that miR-507 regulated Flt-1 expression through a significant reduction or addition of luciferase activity in cells transfected with miR-507 mimic or miR-507 inhibitor, compared with control cells (NC) (Figure 2C). [score:5]
Clinical information of the samples is described in detail in Table 1. In vivo assays for metastasis For the experimental metastasis mouse xenograft mo del, MDA-MB-231 cells stably expressing miR-507 NC (MDA231/NC), miR-507 mimic lentiviral vector (MDA231/miR507), knocked-down Flt-1 expression (SiFlt-1/MDA231), the negative control (Scr/MDA231) were injected into their mammary fat pads of five-week-old female BALB/C-nu/nu nude mice (N = 10). [score:5]
MDA-MB-231 cells were co -transfected with NC or miR-507 together with pcDNA3.1 or pcDNA3.1-Flt-1 for 48 hours with the stimulation of PlGF-1. Flt-1 overexpression rescued the invasion partially caused by the ectopic expression of miR-507 in MDA-MB-231 (Figure 2F). [score:5]
Hence, miR-507 appeared to negatively regulate tumor invasion and metastasis in breast-cancer patients by targeting Flt-1. Figure 5, and the function of miR-507 A. expression of miR-507 in 30 pairs of frozen invasive ductal carcinoma tissues (T) compared with their corresponding adjacent non-cancerous tissues (ANT). [score:5]
B. Western blot analysis of Flt-1 expression in MDA-MB-231 and MCF-7 cells transfected with miR-507 and miR-507 inhibitor. [score:5]
Moreover, Flt-1 was confirmed to be a direct target gene of miR-507. [score:4]
miR-507 downregulation was due to hypermethylation of the promoter region of the miR-507 gene. [score:4]
Our data demonstrated that the hypermethylation of the upstream promoter of miR-507 led to the down-regulation of miR-507 in breast-cancer tissues and cell lines. [score:4]
These findings imply that miR-507 down-regulation is due to hypermethylation of promoter. [score:4]
Flt-1 promoted the migration and chemotaxis of breast-cancer cells by binding to PlGF-1. In addition, we found a down-regulation of miR-507 in breast-cancer tissues and cells with respect to the adjacent non-neoplastic tissues and normal cells. [score:4]
miR-507 modulates Flt-1 expression and is in turn regulated through promoter methylation. [score:4]
Second, miR-507 was sufficiently strong enough to inhibit Flt-1 via direct binding to the Flt-1 3′-UTR. [score:4]
Functional assays showed that the expression of miR-507 was inversely correlated with the expression of Flt-1 and the invasive potential of breast cancer. [score:4]
In vitro luciferase assay confirmed that miR-507 exerted its effects by targeting Flt-1. We also observed that miR-507 was ubiquitously expressed at lower levels in human breast-cancer cell lines than in MCF-10A cell lines. [score:4]
To elucidate the mechanism of miR-507 down-regulation, we performed BSP with genomic DNA to analyze the methylation level of miR-507. [score:4]
Further analysis showed that the down-regulation of miR-507 in breast cancer was associated with tumor differentiation, lymphatic metastasis, and distant metastasis (Table 1), but it did not correlate with age, tumor size, or hormonal status (Table 1). [score:4]
Taken together, these findings strongly suggest that miR-507 down-regulation was due to hypermethylation in the promoter region of the miR-507 gene. [score:4]
The expression of miR-507 and Flt-1 in breast-cancer tissues, and the function of miR-507. [score:3]
Thus, PlGF-1, Flt-1 and miR-507 may be useful prognostic markers for glioma and novel therapeutic targets for breast cancer. [score:3]
Correlation between clinical features and miR-507 expression in invasive ductal carcinoma patients. [score:3]
Seed sequences of miR-507 and pairing 3′-UTR sequences of Flt-1 were predicted by TargetScan 6.0 and miRNA. [score:3]
We detected the expression of miR-507 in breast-cancer cell lines using qRT-PCR. [score:3]
The results showed that miR-507 was ubiquitously expressed at lower levels in human breast-cancer cell lines than in MCF-10A cell lines (Figure 2A). [score:3]
miR-507 mimics, miR-507 inhibitor and negative control mimics (NC) were synthesized by GenePharma company (Shanghai, China). [score:3]
Both our in vitro and in vivo results support that miR-507 significantly inhibits the invasion and metastasis of invasive ductal carcinoma. [score:3]
Figure 2, and A. Expression of miR-507 in breast-cancer cell lines through qRT-PCR analysis. [score:3]
To further examine the role of miR-507 on human primary tumors, we studied miR-507 expression in 90 archived paraffin-embedded specimens of invasive ductal carcinoma and 30 selected frozen (liquid nitrogen) invasive ductal carcinoma tissues and adjacent non-tumor (ANT) tissues using qRT-PCR. [score:3]
The expression of miR-507 and Flt-1 in breast-cancer tissues. [score:3]
These findings demonstrate that miR-507 may function as a tumor suppressor gene in invasive ductal carcinoma. [score:3]
These data are consistent with most of the previous research, further suggesting that miR-507 may perform a tumor-suppressive function. [score:3]
Flt-1 promoted lung colonization of human breast cancer with PlGF-1 stimulation, and miR-507 inhibited lung colonization of human breast cancer in animal experiments. [score:3]
Flt-1 promoted lung colonization of human breast cancer with PlGF-1 stimulation, and miR-507 inhibited lung colonization of human breast cancer in vivo. [score:3]
miR-507 inhibited PlGF-1 -induced invasion, chemotaxis, and actin polymerization of breast-cancer cells. [score:3]
B. In human breast-cancer tissues, miR-507 has a negative correlation with Flt-1 protein expression. [score:3]
miR-507 inhibited PlGF-1 -induced chemotaxis and actin polymerization of breast-cancer cells. [score:3]
We found that the miR-507 expression level was lower in invasive ductal carcinoma tissues than that in ANT tissues (Figure 5A). [score:3]
Overall, the above results suggest that Flt-1 is a functional target of miR-507, contributing to invasion in MDA-MB-231 cells. [score:3]
Our results showed that miR-507 participated in PlGF-1 -induced F-actin polymerization to mediate cytoskeletal rearrangement by inhibiting phosphorylation of LIMK and cofilin, which is essential for cell migration [20, 21]. [score:3]
To find more evidence, we treated MCF-10A, MCF-7, and MDA-MB-231 cells with 5 μM 5-aza-dC for 72 h and found that miR-507 expression was significantly increased in MCF-7 and MDA-MB-231 cells (Figure 5D). [score:3]
Flt-1 promoted lung colonization of human breast cancer with PlGF-1 stimulation, and miR-507 inhibited lung colonization of human breast cancer in vivoThe metastatic properties of breast-cancer cells were analyzed in vivo through a xenograft transplant mo del in SCID mice. [score:3]
In addition, the inverse correlation between miR-507 and Flt-1 expression is evidenced in our clinical analysis. [score:3]
By transfecting miR-507 into MDA-MB-231 and MCF-7 cells, we demonstrated that miR-507 could significantly repress Flt-1 protein expression and affect breast-cancer invasion. [score:3]
Furthermore, low miR-507 expression in breast cancer depends on the hypermethylation of its DNA promoter. [score:3]
A. Expression of miR-507 in breast-cancer cell lines through qRT-PCR analysis. [score:3]
Figure 4Flt-1 promoted lung colonization of human breast cancer with PlGF-1 stimulation, and miR-507 inhibited lung colonization of human breast cancer in vivo A. Human tumor foci in mouse lungs were visualized by H&E staining. [score:3]
The results were consistent with the in vitro findings and indicated that Flt-1 induced the invasion of breast cancer by binding to PlGF-1, and miR-507 inhibited the invasion of breast cancer. [score:3]
The results showed that Flt-1 expression decreased significantly in miR-507 -transfected cells, but increased in ant-miR-507 transfected cells compared with the control cells (Figure 2B). [score:2]
An F-actin polymerization assay was done to verify that miR-507 over -expression influenced breast-cancer cell migration by reducing F-actin polymerization. [score:2]
A more than 50% reduction in expression in primary esophageal squamous cell carcinoma (ESCC) tissue was compared with the corresponding noncancerous tissue and was observed in nine cases (30.0%) for miR-507 [18]. [score:2]
MiR-507 inhibited PlGF-1 -induced chemotaxis and actin polymerization of breast-cancer cells. [score:2]
Analysis of PlGF-1 -induced phosphorylation of LIMK and cofilin in MDA231/miR-507 cells showed a marked inhibit activation of both cofilin and LIMK, compared with MDA231/NC cells, whereas both total LIMK and cofilin levels remained unchanged (Figure 3F). [score:2]
We injected Scr/MDA231, SiFlt-1/MDA231, MDA231/NC, and MDA231/miR-507 cells into the mammary fat pads of SCID mouse. [score:1]
D. qRT-PCR analysis of miR-507 expression in indicated cells treated with 5 μM 5-aza-dC or DMSO for 72 h. Columns, mean of triplicate measurements. [score:1]
A DNA fragment containing the hsa-miR-507 precursor with 300 bp flanking sequence of each side was amplified into retroviral transfer plasmid pMSCV-puro (GenePharma Company, Shanghai, China). [score:1]
All reactions were carried out in triplicate, and the 2 [−ΔΔCt] method (ΔCT = CT [miR-507] - CT [U6]) was used to quantify the relative amount of miR-507. [score:1]
F. Western blot analysis of the phosphorylation of cofilin and LIMK in total cell lysates from MDA231/NC and MDA231/miR-507 cells with 10 ng/mL PlGF-1 stimulation for 0 min, 5 min, and 10 min. [score:1]
To investigate the contribution of miR-507 to invasion, we ectopically expressed miR-507 together with Flt-1 in MDA-MB-231 cells to evaluate whether Flt-1 may overcome the suppressing effect of miR-507 on cell invasion. [score:1]
C. Comparison of chemotactic responses with rPlGF-1 stimulation in MCF-7, NC/MCF-7, and anti-miR-507/MCF-7. The data were collected in this set of figures from a representative of at least three independent experiments. [score:1]
The pGL3 construct and the miR-507 mimic, control mimic or miR-507 mutant were co -transfected into cells cultured using Lipofectamine 2000. [score:1]
D. Time course of relative F-actin content in MDA231/NC cells and MDA231/miR-507 cells with rPlGF-1 stimulation. [score:1]
B. Comparison of chemotactic responses with rPlGF-1 stimulation in MDA-MB-231, MDA231/NC, and MDA231/miR-507. [score:1]
The results showed that the methylation levels of miR-507 were significantly higher in both breast-cancer cell lines and tissues than in immortalized human breast epithelial cell lines (MCF-10A) and ANT. [score:1]
Our results showed that Flt-1 binding to PlGF-1 played an important role in breast-cancer cell migration and chemotaxis that is modulated by miR-507. [score:1]
In addition, the methylation levels of miR-507 in MCF-7 cells (low metastasis cell line) were lower than those in MDA-MB-231 cells (high metastasis cell line) (Figure 5C). [score:1]
Chi-square test was used to analyze the relationship between miR-507 expression and the clinicopathologic characteristics. [score:1]
The immunofluorescent staining of the F-actins showed that the PlGF-1 induced an increase in the F-actin contents of the MDA231/NC cells, but not of the MDA231/miR-507 cells (Figure 3E). [score:1]
C. Methylation level of the miR-507 genomic region in MCF-10A, breast-cancer cell lines (MCF-7 and MDA-MB-231), breast-cancer tissues (T), and their corresponding adjacent non-cancerous tissues (ANT). [score:1]
Finally, Flt-1 is inversely correlated with miR-507. [score:1]
Based on these findings, the methylation status of miR-507 probably acts as a potential biomarker for breast-cancer prognosis. [score:1]
Until now, the roles of miR-507 in breast cancer have never been described, and this prompted us to identify and validate the role of miR-507 in breast cancer. [score:1]
C. Western blot analysis for Flt-1 in slices of sectioned implanted tumors; the mice were injected with Scr/MDA231, SiFlt-1/MDA231, MDA231/NC, and MDA231/miR-507 cells. [score:1]
Overall, all results indicate that miR-507 plays an important role in the PlGF-1 induced LIMK and cofilin recycling. [score:1]
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2
[+] score: 129
The JJ012/vector, JJ012/shCCL5, JJ012/CCL5, SW1353/vector, SW1353/shCCL5 and SW1353/CCL5 cells cultured for 24 h, and miR-507 expression was examined by qPCR A. In addition, cells were transfected with miR-507 mimic or inhibitor for 24 h, and VEGF-C expression was examined by qPCR B. ELISA C. and Western blot E. (n = 5-7). [score:7]
As shown in Figure 3A, the miR-507 was downregulated in JJ012/CCL5 and SW1353/CCL5 cells, and upregulated in JJ012/shCCL5 and SW1353/shCCL5 cells. [score:7]
Strikingly, we revealed that miR-507 directly inhibited VEGF-C protein expression through binding to the 3′UTR of the human VEGF-C gene, thereby negatively regulating VEGF-C -mediated lymphangiogenesis. [score:7]
Figure 3The JJ012/vector, JJ012/shCCL5, JJ012/CCL5, SW1353/vector, SW1353/shCCL5 and SW1353/CCL5 cells cultured for 24 h, and miR-507 expression was examined by qPCR A. In addition, cells were transfected with miR-507 mimic or inhibitor for 24 h, and VEGF-C expression was examined by qPCR B. ELISA C. and Western blot E. (n = 5-7). [score:7]
miR-507 has been shown to suppress the NF-E2-related factor 2 (NRF2) -mediated oncogenic pathway by directly targeting NRF2 [41]. [score:6]
We confirmed miR-507 expression using quantitative real-time PCR (qPCR) in both CCL5 -overexpressed and CCL5-knockdowned cells. [score:6]
The miR-507 inhibits VEGF-C expression through binding to the 3′UTR of human VEGF-C. CCL5 boosts tumor -associated lymphangiogenesis by down -regulating miR-507. [score:6]
To explore the role of miR-507 in CCL5 -induced VEGF-C production and lymphangiogenesis, we transiently transfected the miR-507 mimic or miR-507 inhibitor into CCL5 -overexpressed cells and CCL5-knockdowned cells, respectively. [score:6]
To validate the effect and targeting miRNA of CCL5 on tumor lymphangiogenesis, we analyzed the expression of CCL5, VEGF-C and miR-507 in tumor tissues which were excised from chondrosarcoma xenograft mice. [score:5]
In order to verify whether miR-507 regulates the 3′UTR of VEGF-C, we constructed luciferase reporter vectors harboring wildtype 3′UTR of VEGF-C mRNA (wt-VEGFC-3′UTR) and vector containing mismatches in the predicted miR-507 binding site (mt-VEGFC-3′UTR) and transfected these vectors into CCL5 -overexpressed cells, CCL5-knockdowned cells and control cells. [score:5]
Figure 4The miR-507 inhibits VEGF-C expression through binding to the 3′UTR of human VEGF-C A. Schematic representation of the 3′UTR of the human VEGF-C containing a miR-507 binding site. [score:5]
This kit contained 384 human miRNA primer, we analyzed 33 metastatic miRNA and found the miR-507 was the most downregulated in response to CCL5 overexpression (Supplementary Figure 4). [score:5]
To our knowledge, this study is first time to indicate that miR-507 negatively regulates VEGF-C expression. [score:4]
Figure 6 CCL5 promotes VEGF-C production by downregulating miR-507 in human chondrosarcoma cells, and subsequently induces lymphangiogenesis of human LECs. [score:4]
Taken together, these findings demonstrate that miR-507 directly represses VEGF-C expression via binding to 3′UTR of the human VEGF-C gene. [score:4]
CCL5 promotes VEGF-C production by downregulating miR-507 in human chondrosarcoma cells, and subsequently induces lymphangiogenesis of human LECs. [score:4]
Current study showed that CCL5 markedly repressed miR-507 expression in human chondrosarcoma cells in vitro and in vivo. [score:3]
Figure 5CCL5 promotes tumor lymphangiogenesis by suppressing miR-507 in vivoThe JJ012/vector, JJ012/shCCL5 and JJ012/CCL5 cells were mixed with Matrigel and injected into flank sites of mice (n = 8-10) for six weeks. [score:3]
Importantly, we further demonstrate that CCL5 promotes VEGF-C -mediated tumor lymphangiogenesis by suppressing miR-507 in human chondrosarcoma. [score:3]
In the series of experiments, stable cell lines were incubated alone or transfected with miR-507 mimic or inhibitor for 24 h. After treatment, cells were washed and changed to serum-free medium. [score:3]
Moreover, administration of miR-507 alone or in combination with cisplatin significantly inhibits tumor growth in esophageal squamous cell carcinoma. [score:3]
The miR-507 mimic, miR-507 inhibitor, Lipofectamine 2000 and Trizol were purchased from Life Technologies (Carlsbad, CA, USA). [score:3]
We found that cotransfection with the miR-507 mimic inhibited luciferase activity in the wt-VEGFC-3′UTR plasmid but not in the mt-VEGFA-3′UTR plasmid (Figure 4). [score:3]
CCL5 promotes tumor lymphangiogenesis by suppressing miR-507 in vivo. [score:3]
CCL5 promotes VEGF-C -dependent lymphangiogenesis by suppressing miR-507. [score:3]
We reveal that CCL5 increases the production of lymphangiogenic factor VEGF-C by down -regulating miR-507 in chondrosarcoma cells, and thereby promotes tumor lymphangiogenesis in chondrosarcoma microenvironment (Figure 6). [score:2]
CCL5 enhances VEGF-C production and lymphangiogenesis by down -regulating miR-507. [score:2]
Therefore, we suggest that CCL5 promotes VEGF-C -dependent tumor -associated lymphangiogenesis by down -regulating miR-507 in vivo. [score:2]
In addition, the miR-507 mimic clearly diminished the CCL5 -induced VEGF-C production and LECs tube formation in JJ012/CCL5 and SW1353/CCL5 cells (Figure 3B-3E). [score:1]
The quantitative data exhibited the positive correlation between CCL5 and VEGF-C, and the negative correlation between CCL5 and miR-507 using qPCR analysis in tumor specimens form animals (Figure 5B& 5C). [score:1]
The 3′-UTR-luciferase reporter constructs containing the 3′-UTR regions of VEGF-C with wild-type and mutant binding sites for miR-507 were amplified using the PCR method. [score:1]
Cotransfection of cells with miR-507 mimic abolished CCL5 -induced VEGF-C production and LECs tube formation. [score:1]
A. Schematic representation of the 3′UTR of the human VEGF-C containing a miR-507 binding site. [score:1]
org), and found that the 3′-UTR of VEGF-C mRNA harbors potential binding sites for miR-507. [score:1]
The data showed that VEGF-C production and LECs tube formation were obviously reduced by the miR-507 mimic in JJ012/shCCL5 and SW1353/shCCL5 cells. [score:1]
Then, the xenografted tumors were excised and stained with CCL5, VEGF-C and LYVE-1 by IHC A. The correlation between CCL5/VEGF-C B. and CCL5/miR-507 C. in tumor tissues was analyzed by qPCR and Spearman rank correlation test (n = 8) (R [2] > 0.5). [score:1]
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3
[+] score: 35
Through qPCR, we found that the expression levels of these three miRNAs were all significantly down-regulated in mutant type (rs5951785 near hsa-miR-506, P=4.47×10 [−2], Figure 1A; rs5951785 near hsa-miR-507, P=4.80×10 [−3], Figure 2A; rs1447393 near hsa-miR-510, P=3.00×10 [−4], Figure 3A). [score:6]
The miR-507 expression level was significant down-regulated in mutant type compared with the wild type. [score:5]
A. RT-PCR was applied to detected mature miR-507 expression levels. [score:3]
However, we didn't observe apoptosis changes after overexpress hsa-miR-507. [score:3]
ADAM17, a target of miR-507, is involved in germ cell apoptosis during spermatogenesis [20]. [score:3]
Figure 2 A. RT-PCR was applied to detected mature miR-507 expression levels. [score:3]
Besides, we also found hsa-miR-506 mutant-type significantly increased cell apoptosis (P=1.69×10 [−2], Figure 1D, 1E), while there was no difference in hsa-miR-507 nor hsa-miR-510 between the wild and mutant alleles (Figure 2D, 2E; Figure 3D, 3E), implicating that growth inhibition was accompanied with increased apoptosis population. [score:3]
There was no significant difference of cell apoptosis in rs5951785 near miR-507. [score:1]
Functional analysis demonstrated that rs5951785 near miR-507 might contribute to the risk of NOA. [score:1]
No significant difference was observed in cell proliferation of the rs5951785 near miR-507. [score:1]
It was significantly increased in miR-507 mutant type for ADAM17. [score:1]
Through conducting dual-luciferase reporter assay, we found that the luciferase activities of CDK4, GLI3, PIK3C2A, ADAM17, SFRP2 and PRDX1 were significantly decreased when compared to the vectors, suggesting that they were the potential targets of hsa-miR-506, hsa-miR-507 and hsa-miR-510, respectively (Figure 1B, 2B, 3B). [score:1]
C. CCK8 was used to determine the influence of rs5951785 near miR-507 on cell growth. [score:1]
No significant difference was observed in the rs5951785 near hsa-miR-507 (Figure 2C). [score:1]
F, G. Effects of rs5951785 near miR-507 on cell cycle were analyzed with flow cytometry. [score:1]
There was no difference of cell cycle between miR-507 wild and miR-507 mutant type. [score:1]
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4
[+] score: 8
For the efficient target LEF1, miR-507 repressed it only in CIN I stage, and it had contribution to the processes of ‘Wnt signaling pathway’, ‘embryonic limb morphogenesis’, ‘positive regulation of epithelial to mesenchymal transition’, ‘mammary gland development’, ‘tongue development’, and ‘paraxial mesoderm formation’ only in CIN III stage. [score:6]
Based on this, our finding suggests that miR-507’s differential regulation on LEF1, may lead to cell poor differentiation in CIN III stage. [score:2]
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5
[+] score: 7
Induction of miR-506 and miR-507 expression was greatly attenuated by low doses of α-amanitin (Figure 3A and B), which selectively targets RNA pol II -dependent transcription. [score:5]
The miRNAs included miR-506, miR-507, miR-508, miR-513a-1, miR-513a-2 (highly homologous miR-513a-1 and miR-513a-2 were indistinguishable by array hybridization. [score:1]
For the same reason the fold induction of miR-507 could not been estimated in the high-throughput sequencing experiment. [score:1]
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6
[+] score: 7
Other miRNAs from this paper: hsa-mir-22, hsa-mir-140, hsa-mir-188, hsa-mir-372
In fact, UCA1 might act as a decoy lncRNA targeting miR-507, an inhibitor of the pro-oncogenic transcription factor FoxM1 (Figure 1A). [score:5]
Wei Y. Sun Q. Zhao L. Wu J. Chen X. Wang Y. Zang W. Zhao G. LncRNA UCA1-miR-507-FOXM1 axis is involved in cell proliferation, invasion and G0/G1 cell cycle arrest in melanomaMed. [score:1]
Depletion of UCA1 increased the levels of miR-507 and reduced FoxM1 levels which led to cell cycle progression defects [125]. [score:1]
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7
[+] 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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8
[+] score: 4
miR-21 and miR-223 expression levels were increased in TGCTs, whereas the eight miRNAs in the miR-506~514 cluster (miR-506, miR-507, miR-508-5p, miR-510, miR-513a-5p, miR-513b, miR-513c and miR-514a-3p) were reduced in TGCTs as compared with NT. [score:2]
This cluster is conserved in primates, and consists of seven distinct miRNAs, that is, miR-506, miR-507, miR-508, miR-509, miR-510, miR-513 and miR-514. [score:1]
For mature miRNAs, cDNA was synthesized from 150 ng of total RNA and used to quantitate miR-506 (ID 001050), miR-510 (ID 002241), miR-514a-3p (ID 242955_mat), miR-513c (ID 002756), miR-513b (ID 002757), miR-513a-5p (ID 002090), miR-507 (ID 001051), miR-508-5p (ID 002092), miR-21 (ID 000397), miR-223 (ID 002295), miR-372 (ID 000560) and miR-373 (ID 000561). [score:1]
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9
[+] score: 4
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-16-1, 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-92a-1, hsa-mir-92a-2, hsa-mir-106a, hsa-mir-16-2, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181a-1, hsa-mir-221, hsa-mir-222, hsa-mir-223, hsa-let-7g, hsa-let-7i, hsa-mir-15b, hsa-mir-23b, hsa-mir-27b, hsa-mir-122, hsa-mir-125b-1, hsa-mir-140, hsa-mir-125b-2, hsa-mir-136, hsa-mir-146a, hsa-mir-150, hsa-mir-206, hsa-mir-155, hsa-mir-181b-2, hsa-mir-106b, hsa-mir-302a, hsa-mir-34b, hsa-mir-34c, hsa-mir-302b, hsa-mir-302c, hsa-mir-302d, hsa-mir-367, gga-let-7i, gga-let-7a-3, gga-let-7b, gga-let-7c, gga-mir-125b-2, gga-mir-155, gga-mir-222a, gga-mir-221, gga-mir-92-1, gga-mir-19b, gga-mir-20a, gga-mir-19a, gga-mir-18a, gga-mir-17, gga-mir-16-1, gga-mir-15a, gga-mir-1a-2, gga-mir-206, gga-mir-223, gga-mir-106, gga-mir-302a, gga-mir-181a-1, gga-mir-181b-1, gga-mir-16-2, gga-mir-15b, gga-mir-140, gga-let-7g, gga-let-7d, gga-let-7f, gga-let-7a-1, gga-mir-146a, gga-mir-181b-2, gga-mir-181a-2, gga-mir-1a-1, gga-mir-1b, gga-let-7a-2, gga-mir-34b, gga-mir-34c, gga-let-7j, gga-let-7k, gga-mir-23b, gga-mir-27b, gga-mir-24, gga-mir-122-1, gga-mir-122-2, hsa-mir-429, hsa-mir-449a, hsa-mir-146b, hsa-mir-455, hsa-mir-92b, hsa-mir-449b, gga-mir-146b, gga-mir-302b, gga-mir-302c, gga-mir-302d, gga-mir-455, gga-mir-367, gga-mir-429, gga-mir-449a, hsa-mir-449c, gga-mir-21, gga-mir-1458, gga-mir-1576, gga-mir-1612, gga-mir-1636, gga-mir-449c, gga-mir-1711, gga-mir-1729, gga-mir-1798, gga-mir-122b, gga-mir-1811, gga-mir-146c, gga-mir-15c, gga-mir-449b, gga-mir-222b, gga-mir-92-2, gga-mir-125b-1, gga-mir-449d, gga-let-7l-1, gga-let-7l-2, gga-mir-122b-1, gga-mir-122b-2
Another two human miRNAs (miR-507 and miR-136) have potential target binding sites in polymerase basic 2 (PB2) and hemagglutinin (HA) genes of AIV, respectively [15]. [score:3]
Two human encoded miRNAs (miR-136 and miR-507), have been shown to have potential binding sites for the genes that code for the polymerase basic 2 (PB2) and hemmagglutinin (HA) proteins and are reported to be involved in the pathogenesis of H5N1 AIV [15]. [score:1]
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10
[+] score: 3
Influenza virus infection modulates multiple cellular miRNAs, and miR-323, miR-491, and miR-654 have been shown to inhibit viral replication by binding to the viral PB1 gene [48], while miR-507 and miR-136 have potential binding sites within the viral PB2 and HA genes [49]. [score:3]
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11
[+] score: 3
Finally, our analysis identified a cluster of testis-enriched miRNAs located on chromosome X, including miR-506, miR-507, miR-508 and miR-514, that was previously reported as preferentially expressed in testis [32]. [score:3]
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12
[+] score: 3
MiR-507 and miR-136 could restrict the virus replication by targeting the genes of influenza virus Polymerase B2 (PB2) and Hemagglutinin (HA), respectively [15]. [score:3]
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13
[+] score: 2
On the other hand the role of miR-9, miR-148b, miR-203 and miR-507 in HCC pathobiology is not well understood. [score:1]
Finally, nothing is known regarding the role of miR-507 in HCC pathogenesis. [score:1]
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14
[+] 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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15
[+] score: 1
Based on computational prediction, human miR-136 and miR-507 have potential binding sites at the polymerase basic 2 (PB2) and hemmagglutinin (HA) proteins of H5N1 AIV, and those two miRNAs may modulate AIV infection in humans [19]. [score:1]
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16
[+] score: 1
Only one of these (pal-can-332) shares 100% mature sequence identity with a known vertebrate miRNA (miR-507), while the remaining 14 are unique to P. alecto. [score:1]
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17
[+] score: 1
In particular six out of eight chrXq27.3 miRNAs (miR-506, miR-507, miR-508-3p, miR-509-3p, miR-509-5p and miR-514) showed Pearson’s correlation greater than 0.95 (Figure 4A). [score:1]
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18
[+] score: 1
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-17, hsa-mir-21, hsa-mir-29a, hsa-mir-96, mmu-let-7g, mmu-let-7i, mmu-mir-124-3, mmu-mir-140, mmu-mir-181a-2, mmu-mir-182, mmu-mir-183, mmu-mir-194-1, mmu-mir-200b, hsa-mir-34a, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-182, hsa-mir-183, hsa-mir-181a-1, hsa-mir-200b, mmu-mir-34c, mmu-mir-34b, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-140, hsa-mir-194-1, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-15a, mmu-mir-21a, mmu-mir-29a, mmu-mir-96, mmu-mir-34a, mmu-mir-135b, hsa-mir-200c, hsa-mir-181b-2, mmu-mir-17, mmu-mir-200c, mmu-mir-181a-1, mmu-mir-124-1, mmu-mir-124-2, mmu-mir-181b-1, mmu-mir-181c, hsa-mir-194-2, mmu-mir-194-2, hsa-mir-34b, hsa-mir-34c, hsa-mir-376c, hsa-mir-376a-1, mmu-mir-376a, hsa-mir-135b, mmu-mir-181b-2, mmu-mir-376b, dre-mir-34a, dre-mir-181b-1, dre-mir-181b-2, dre-mir-182, dre-mir-183, dre-mir-181a-1, dre-let-7a-1, dre-let-7a-2, dre-let-7a-3, dre-let-7a-4, dre-let-7a-5, dre-let-7a-6, dre-let-7b, dre-let-7c-1, dre-let-7c-2, dre-let-7d-1, dre-let-7d-2, dre-let-7e, dre-let-7f, dre-let-7g-1, dre-let-7g-2, dre-let-7h, dre-let-7i, dre-mir-15a-1, dre-mir-15a-2, dre-mir-17a-1, dre-mir-17a-2, dre-mir-21-1, dre-mir-21-2, dre-mir-29a, dre-mir-96, dre-mir-124-1, dre-mir-124-2, dre-mir-124-3, dre-mir-124-4, dre-mir-124-5, dre-mir-124-6, dre-mir-140, dre-mir-181c, dre-mir-194a, dre-mir-194b, dre-mir-200b, dre-mir-200c, hsa-mir-376b, hsa-mir-181d, dre-let-7j, dre-mir-135b, dre-mir-181a-2, hsa-mir-376a-2, mmu-mir-376c, dre-mir-34b, dre-mir-34c, mmu-mir-181d, mmu-mir-21b, mmu-let-7j, mmu-mir-21c, mmu-let-7k, dre-mir-181a-4, dre-mir-181a-3, dre-mir-181a-5, dre-mir-181b-3, dre-mir-181d, mmu-mir-124b
A variant was found in an Iranian family, c. *95C>A, predicted to alter the binding site of miR-96/182 and create a new miRNA binding site for miR-507 and -557. [score:1]
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