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miR‐150 promotes the proliferation of lung cancer cells by targeting P53
Author(s) -
Zhang Ni,
Wei Xiang,
Xu Lijun
Publication year - 2013
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2013.05.059
Subject(s) - lung cancer , cancer research , pathogenesis , suppressor , downregulation and upregulation , cancer , cell growth , biology , apoptosis , microrna , tumor suppressor gene , cancer cell , gene , carcinogenesis , medicine , immunology , pathology , genetics
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.