miR-134 inhibits epithelial to mesenchymal transition by targeting FOXM1 in non-small cell lung cancer cells

被引:151
作者
Li, Jipeng [2 ]
Wang, Yiping [2 ]
Luo, Jianping [2 ]
Fu, Zhongming [1 ]
Ying, Jianfei [2 ]
Yu, Yanhong [2 ]
Yu, Wanjun [1 ,2 ]
机构
[1] Yinzhou Peoples Hosp, Dept Resp Dis, Ningbo 315040, Zhejiang, Peoples R China
[2] Yinzhou Peoples Hosp, Dept Clin Lab, Ningbo 315040, Zhejiang, Peoples R China
关键词
miR-134; Epithelial-to-mesenchymal transition (EMT); NSCLC; FOXM1; TGF-beta; 1; M1 TRANSCRIPTION FACTOR; EXPRESSION; GROWTH; FAMILY; MECHANISMS; INVASION; LEADS;
D O I
10.1016/j.febslet.2012.09.016
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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-beta 1-induced EMT in A549 cells. These findings suggest that miR-134 acts as a novel EMT suppressor in NSCLC cells. (C) 2012 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
引用
收藏
页码:3761 / 3765
页数:5
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