miR-150 promotes the proliferation of lung cancer cells by targeting P53

被引:148
作者
Zhang, Ni [1 ]
Wei, Xiang [2 ]
Xu, Lijun [2 ]
机构
[1] Huazhong Univ Sci & Technol, Dept Throrac Surg, Tongji Hosp, Tongji Med Coll, Wuhan 430030, Peoples R China
[2] Huazhong Univ Sci & Technol, Dept Cardiothrorac Surg, Tongji Hosp, Tongji Med Coll, Wuhan 430030, Peoples R China
关键词
miR-150; P53; Cell proliferation; Lung cancer; DNA-DAMAGE; MICRORNA; PATHOGENESIS; APOPTOSIS; TUMORIGENESIS; PROGNOSIS; MIRNAS; GENE;
D O I
10.1016/j.febslet.2013.05.059
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
070307 [化学生物学]; 071010 [生物化学与分子生物学];
摘要
Lung cancer is one of the most common causes for cancer-related death. Previous studies suggested that uncontrolled cell proliferation induced by activation of pro-cancer genes or inhibition of cancer suppressor genes plays an important role in the pathogenesis of lung cancer. Here, we demonstrate that miR-150 is aberrantly upregulated in lung cancer tissue and negatively correlates with the expression of the proapoptotic gene p53 but not EGR2. We show that miR-150 specifically targets the 3'-UTR of p53 and regulates its expression. Inhibition of miR-150 effectively delays cell proliferation and promotes apoptosis, accompanied by increased p53 protein expression. Our data reveals the mechanisms underlying miR-150 regulated lung cancer pathogenesis, which might be beneficial for lung cancer therapy. (C) 2013 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
引用
收藏
页码:2346 / 2351
页数:6
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