Huang Haili, Hu Min, Li Peng, Lu Caijie, Li Mingyi
Clinical Research Center, the Affiliated Hospital of Guangdong Medical College, 524001, Zhanjiang, China.
Tumour Biol. 2015 Feb;36(2):921-8. doi: 10.1007/s13277-014-2719-x. Epub 2014 Oct 15.
miR152 is involved in diverse biological functions and development of disease. This study investigates the role of mir-152 in cell proliferation and colony formation of liver cancer stem cells. We show that exogenous overexpression of mir-152 suppresses cell proliferation and colony formation in CD133(+) hep3B cells. We also show that KIT is a direct target of miR-152 and miR-152 downregulates protein expression of KIT by directly binding to 3' untranslated region of KIT. Downregulation of KIT by specific siRNAs inhibits proliferation and colony formation of CD133(+) hep3B cells, which is similar to inhibitory effects of miR-152. Moreover, exogenous expression of KIT compromises inhibitory effects of miR-152 on cell proliferation and colony formation. Our findings suggest that mir-152 inhibits cell proliferation and colony formation of CD133(+) hep3B cells by targeting KIT.
miR152参与多种生物学功能及疾病发展。本研究调查了mir-152在肝癌干细胞的细胞增殖和集落形成中的作用。我们发现,mir-152的外源性过表达抑制了CD133(+) hep3B细胞的细胞增殖和集落形成。我们还表明,KIT是miR-152的直接靶点,且miR-152通过直接结合KIT的3'非翻译区下调KIT的蛋白表达。用特异性小干扰RNA(siRNAs)下调KIT可抑制CD133(+) hep3B细胞的增殖和集落形成,这与miR-152的抑制作用相似。此外,KIT的外源性表达削弱了miR-152对细胞增殖和集落形成的抑制作用。我们的研究结果表明,mir-152通过靶向KIT抑制CD133(+) hep3B细胞的细胞增殖和集落形成。