| Literature DB >> 24381057 |
Qingliang Zheng1, Qing Sheng, Caiying Jiang, Jianhong Shu, Jian Chen, Zuoming Nie, Zhengbing Lv, Yaozhou Zhang.
Abstract
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.Entities:
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Year: 2014 PMID: 24381057 DOI: 10.1007/s11010-013-1940-z
Source DB: PubMed Journal: Mol Cell Biochem ISSN: 0300-8177 Impact factor: 3.396