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miR‐137 inhibits the proliferation of lung cancer cells by targeting Cdc42 and Cdk6
Author(s) -
Zhu Xiaolan,
Li Yuefeng,
Shen Huiling,
Li Hao,
Long Lulu,
Hui Lulu,
Xu Wenlin
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.2012.11.004
Subject(s) - cyclin dependent kinase 6 , cancer research , carcinogenesis , lung cancer , ectopic expression , downregulation and upregulation , microrna , cell growth , dna methylation , cdc42 , cell cycle , biology , cancer , microbiology and biotechnology , medicine , kinase , cell culture , pathology , gene expression , cyclin dependent kinase 2 , gene , genetics
MicroRNAs (miRNA) have emerged as key players in carcinogenesis. Here, we investigated the role of miR‐137 in the pathogenesis of lung cancer. The downregulation of miR‐137 in lung cancer cells could be rescued following inhibition of DNA methylation. Ectopic expression of miR‐137 in lung cancer cells significantly downregulated Cdc42, Cdk6 and induced G1 cell cycle arrest, leading to a significant decrease in cell growth in vivo and in vitro. Further, both Cdc42 and Cdk6 were confirmed as targets of miR‐137.