Journal
FEBS LETTERS
Volume 587, Issue 15, Pages 2346-2351Publisher
WILEY
DOI: 10.1016/j.febslet.2013.05.059
Keywords
miR-150; P53; Cell proliferation; Lung cancer
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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.
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