Suppr超能文献

Mir-152通过靶向KIT抑制CD133(+)肝癌干细胞的细胞增殖和集落形成。

Mir-152 inhibits cell proliferation and colony formation of CD133(+) liver cancer stem cells by targeting KIT.

作者信息

Huang Haili, Hu Min, Li Peng, Lu Caijie, Li Mingyi

机构信息

Clinical Research Center, the Affiliated Hospital of Guangdong Medical College, 524001, Zhanjiang, China.

出版信息

Tumour Biol. 2015 Feb;36(2):921-8. doi: 10.1007/s13277-014-2719-x. Epub 2014 Oct 15.

Abstract

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.

摘要

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。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验