Premium
miR‐134 inhibits epithelial to mesenchymal transition by targeting FOXM1 in non‐small cell lung cancer cells
Author(s) -
Li Jipeng,
Wang Yiping,
Luo Jianping,
Fu Zhongming,
Ying Jianfei,
Yu Yanhong,
Yu Wanjun
Publication year - 2012
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.2012.09.016
Subject(s) - foxm1 , epithelial–mesenchymal transition , gene knockdown , a549 cell , suppressor , microrna , cancer research , transition (genetics) , phenotype , lung cancer , chemistry , microbiology and biotechnology , cell , biology , oncology , medicine , cell cycle , gene , biochemistry
Recent studies have implied that miRNAs act as crucial modulators for epithelial‐to‐mesenchymal transition (EMT). We found that miR‐134 expression correlated with invasive potential and EMT phenotype of NSCLC cells. Functional assays demonstrated that miR‐134 inhibited EMT in NSCLC cells. In addition, we showed that Forkhead Box M1 (FOXM1) is a direct target of miR‐134. Knockdown of FOXM1 reversed EMT resembling that of miR‐134 overexpression. We further found that FOXM1 was involved in TGF‐β1‐induced EMT in A549 cells. These findings suggest that miR‐134 acts as a novel EMT suppressor in NSCLC cells.