Bo Liu1, Ting Sun1, Gang Wu1, Hui Shang-Guan2, Zhao-Jin Jiang1, Ji-Ren Zhang1, Yan-Fang Zheng1. 1. Oncology Center, Zhujiang Hospital of Southern Medical University Guangzhou 510282, Guangdong, China. 2. Department of Oncology, Foshan Hospital, Southern Medical University Foshan 528000, Guangdong, China.
Abstract
PURPOSE: This study aimed to determine the function of miR-15a in HCC, and identify cMyb as a target of miR-15a. METHODS: RNA expression was evaluated by quantitative real-time PCR (qRT-PCR). The effects of miR-15a or cMyb on HCC cells were evaluated by transwell migration assay and western blot analysis. CMyb, the predicted target, has been frequently verified by luciferase assay. RESULTS: MiR-15a was markedly downregulated in sphere culture HCC cells by qRT-PCR. CMyb was predicted to be a potential target of miR-15a using bioinformatics analysis. This prediction has been frequently verified by luciferase assay and western blot. A positive correlation between cMyb and the migration ability of HCC cells was demonstrated by transwell assays. MiR-15a mimic suppressed cMyb expression to weaken HCC cell migration ability. On the other hand, miR-15a inhibitor upregulated cMyb and induced HCC cell migration. CONCLUSION: MiR-15a could suppress HCC progression through the repression of cMyb, making miR-15a a potential therapeutic target.
PURPOSE: This study aimed to determine the function of miR-15a in HCC, and identify cMyb as a target of miR-15a. METHODS: RNA expression was evaluated by quantitative real-time PCR (qRT-PCR). The effects of miR-15a or cMyb on HCC cells were evaluated by transwell migration assay and western blot analysis. CMyb, the predicted target, has been frequently verified by luciferase assay. RESULTS:MiR-15a was markedly downregulated in sphere culture HCC cells by qRT-PCR. CMyb was predicted to be a potential target of miR-15a using bioinformatics analysis. This prediction has been frequently verified by luciferase assay and western blot. A positive correlation between cMyb and the migration ability of HCC cells was demonstrated by transwell assays. MiR-15a mimic suppressed cMyb expression to weaken HCC cell migration ability. On the other hand, miR-15a inhibitor upregulated cMyb and induced HCC cell migration. CONCLUSION:MiR-15a could suppress HCC progression through the repression of cMyb, making miR-15a a potential therapeutic target.
Authors: Michael F Clarke; John E Dick; Peter B Dirks; Connie J Eaves; Catriona H M Jamieson; D Leanne Jones; Jane Visvader; Irving L Weissman; Geoffrey M Wahl Journal: Cancer Res Date: 2006-09-21 Impact factor: 12.701
Authors: George Adrian Calin; Cinzia Sevignani; Calin Dan Dumitru; Terry Hyslop; Evan Noch; Sai Yendamuri; Masayoshi Shimizu; Sashi Rattan; Florencia Bullrich; Massimo Negrini; Carlo M Croce Journal: Proc Natl Acad Sci U S A Date: 2004-02-18 Impact factor: 11.205