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 VSports手机版. 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. .