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

来源：

FEBS LETTERS | 2012年 / 586卷 / 20期

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

页码：3761 / 3765

页数：5

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