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.
第一作者单位：[1]Huazhong Univ Sci & Technol, Dept Throrac Surg, Tongji Hosp, Tongji Med Coll, Wuhan 430030, Peoples R China
通讯作者：
推荐引用方式(GB/T 7714)：
Zhang Ni,Wei Xiang,Xu Lijun.miR-150 promotes the proliferation of lung cancer cells by targeting P53[J].FEBS LETTERS.2013,587(15):2346-2351.doi:10.1016/j.febslet.2013.05.059.
APA：
Zhang, Ni,Wei, Xiang&Xu, Lijun.(2013).miR-150 promotes the proliferation of lung cancer cells by targeting P53.FEBS LETTERS,587,(15)
MLA：
Zhang, Ni,et al."miR-150 promotes the proliferation of lung cancer cells by targeting P53".FEBS LETTERS 587..15(2013):2346-2351
