Dataset Information

Hsa-mir-1269 genetic variant contributes to hepatocellular carcinoma susceptibility through affecting SOX6.

ABSTRACT: MiR-1269 is an essential oncogene that plays crucial roles in regulating the development of hepatocellular carcinoma (HCC). In this study, we mainly focused on the polymorphisms (rs73239138) in miR-1069 to explore its potential role in regulation of target genes in liver cancer. We detected increased level of miR-1269 in 80 HCC patients. SOX6 was predicted as a potential target gene of miR-as. Notably, Pearson correlation analysis indicated that patients harbored with miR-1269 wild type (rs73239138, GG genotype), positively correlated with SOX6 expression. Over-expression of miR-1269 with GG genotype promoted cell proliferation comparing with AA genotype, which is acompanied by a decreased level of SOX6. Further dual luciferase reporter assay showed that miR-1269 with GG genotype have a stronger binding ability with SOX6. SNP rs73239138 in miR-1269 was very likey to be involved in the development of HCC by acting as a protective factor, as the carriers of GA and GG genotype resulted in a smaller tumor size. In conclusion, our results support that SNP rs73239138 in miR-1269 is a protective factor which prevents binding to 3'UTR of SOX6 and there by suppresses tumor growth in HCC.

SUBMITTER: Xiong G

PROVIDER: S-EPMC4656786 | biostudies-literature | 2015

REPOSITORIES: biostudies-literature

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Hsa-mir-1269 genetic variant contributes to hepatocellular carcinoma susceptibility through affecting SOX6.

Xiong Guanying G Wang Yun Y Ding Quchen Q Yang Lihua L

American journal of translational research 20151015 10

MiR-1269 is an essential oncogene that plays crucial roles in regulating the development of hepatocellular carcinoma (HCC). In this study, we mainly focused on the polymorphisms (rs73239138) in miR-1069 to explore its potential role in regulation of target genes in liver cancer. We detected increased level of miR-1269 in 80 HCC patients. SOX6 was predicted as a potential target gene of miR-as. Notably, Pearson correlation analysis indicated that patients harbored with miR-1269 wild type (rs73239 ...[more]

PMID: 26692953

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Project description:hsa-miR-191 is highly expressed in hepatocellular carcinoma (HCC), but the factors regulating this elevated expression are unknown. This study aimed to investigate the epigenetic mechanisms of increased hsa-miR-191 expression by analyzing the relationship between the DNA methylation status of hsa-miR-191 and miR-191 expression. Methylation-specific polymerase chain reaction (PCR), bisulfite sequencing PCR, Northern blot, and quantitative real-time PCR were performed to examine hsa-miR-191 methylation and expression levels. Western blot, transwell, and scratch assays were performed to examine the function and molecular mechanisms of hsa-miR-191. Approximately 58.9% of hsa-miR-191 expression was higher in HCC tissues than in adjacent noncancerous tissues; this high expression was associated with poor prognosis. The hypomethylation observed in some HCC cell lines and HCC tissues was correlated with the hsa-miR-191 expression level. This correlation was validated by treatment with the 5-aza-DAC demethylation agent. The level of hypomethylation was 63.0% in 73 clinical HCC tissue samples and was associated with increased (2.1-fold) hsa-miR-191 expression. The elevated expression of hsa-miR-191 in the SMMC-771 HCC cell line induced the cells to transition into mesenchymal-like cells; they exhibited characteristics such as loss of adhesion, down-regulation of epithelial cell markers, up-regulation of mesenchymal cell markers, and increased cell migration and invasion. Inhibiting hsa-miR-191 expression in the SMMC-7721 cell line reversed this process (as assessed by cell morphology and cell markers). Furthermore, hsa-miR-191 probably exerted its function by directly targeting TIMP metallopeptidase inhibitor 3 and inhibiting TIMP3 protein expression. Our results suggest that hsa-miR-191 locus hypomethylation causes an increase in hsa-miR-191 expression in HCC clinical tissues and that this expression induces HCC cells to transition into mesenchymal-like cells.

Dataset Information

Hsa-mir-1269 genetic variant contributes to hepatocellular carcinoma susceptibility through affecting SOX6.

Publications

Hsa-mir-1269 genetic variant contributes to hepatocellular carcinoma susceptibility through affecting SOX6.

Similar Datasets

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