Methylation‐mediated repression of microRNA 129‐2 enhances oncogenic SOX4 expression in HCC

摘要: Background & Aims Aberration of miR-129-2 has been linked to a variety human tumours. However, whether is involved in hepatocarcinogenesis remains unknown. Here, we investigate the involvement HBV infection-related HCC. Methods A total 75 paired tumour and their corresponding non-tumour liver tissues from HCC patients with serum HBsAg positive were collected. The methylation gene was quantitatively analysed by DNA methylation-sensitive endonuclease digestion followed quantitative PCR. expression mature (miR-129-3p) detected Taqman RT-PCR. SOX4 using realtime RT-PCR, western blot immunohistochemical staining. function investigated cell proliferation clonogenicity assays vitro. Results Compared adjacent tissues, exhibited significantly increased hypermethylation both frequency (37.33% vs. 8%, P < 0.0001) intensity (14.77% 3.08%, P = 0.002). Accordantly, miR-129-3p lower than that (P = 0.0461), manner reversely correlated level hypermethylation. Notably, higher (P = 0.0174) normal (P = 0.0077), (P = 0.0105). Furthermore, overexpression HepG2 reduced clonogenicity, while co-expression could partially reverse its antitumor effects. In addition, can enhance β-catenin/TCF activity increasing β-catenin level. Conclusion The current data indicated methylation-mediated repression may oncogenic involve tumorigenesis.