MicroRNA-452 promotes tumorigenesis in hepatocellular carcinoma by targeting cyclin-dependent kinase inhibitor 1B

• DOI: 10.1007/s11010-013-1940-z
• Publication Date: 2013-12-31T07:47:08Z
• Authors: Qingliang Zheng; Qing Sheng; Caiying Jiang; Jianhong Shu; Jian Chen; Zuoming Nie; Zhengbing Lv; Yaozhou Zhang
• Keywords: 0301 basic medicine; 0303 health sciences; Carcinoma, Hepatocellular; Carcinogenesis; Liver Neoplasms; G1 Phase; Down-Regulation; Apoptosis; Hep G2 Cells; Cell Line; S Phase; Up-Regulation; MicroRNAs; 03 medical and health sciences; HEK293 Cells; Cell Movement; Cell Line, Tumor; Humans; RNA, Messenger; 3' Untranslated Regions; Cyclin-Dependent Kinase Inhibitor p27; Cell Proliferation

Dysregulation of miR-452 has been observed in many tumors, but its biological function in hepatocellular carcinoma (HCC) is still unknown. Our results showed that miR-452 expression is significantly increased in HCC tissues and HCC cell lines. We also found that overexpression of miR-452 dramatically accelerated proliferation, induced cell cycle from G1 to S transition, and blocked apoptosis of HCC cells. Migration and matrigel invasion assays indicated that miR-452 significantly promotes HepG2 and QGY-7703 cells migration and invasion in vitro. Further studies showed that miR-452 directly targets the 3'-untranslated region of cyclin-dependent kinase inhibitor 1B (CDKN1B), ectopic miR-452 expression suppressed CDKN1B expression on mRNA and protein level. Silencing CDKN1B by small interfering RNA resembled the phenotype resulting from ectopic miR-452 expression. This study provides new insights into the potential molecular mechanisms that miRNA-452 contributed to HCC.