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

• Published in: FEBS letters Vol. 586; no. 20; pp. 3761 - 3765
• Main Authors: Li, Jipeng, Wang, Yiping, Luo, Jianping, Fu, Zhongming, Ying, Jianfei, Yu, Yanhong, Yu, Wanjun
• Format: Journal Article
• Language: English
• Published: England Elsevier B.V 19.10.2012
• Subjects: Base Sequence; Carcinoma, Non-Small-Cell Lung - pathology; Cell Line, Tumor; Epithelial-Mesenchymal Transition - drug effects; Epithelial-Mesenchymal Transition - genetics; Epithelial-to-mesenchymal transition (EMT); Forkhead Box Protein M1; Forkhead Transcription Factors - genetics; FOXM1; Gene Expression Regulation, Neoplastic - drug effects; Humans; lung neoplasms; Lung Neoplasms - pathology; microRNA; MicroRNAs - genetics; MicroRNAs - metabolism; miR-134; neoplasm cells; Neoplasm Invasiveness; NSCLC; phenotype; TGF-β1; Transforming Growth Factor beta1 - pharmacology; TGF-β1; NSCLC; FOXM1; Epithelial-to-mesenchymal transition (EMT); miR-134
• ISSN: 0014-5793; 1873-3468; 1873-3468
• DOI: 10.1016/j.febslet.2012.09.016

► miR-134 correlates with invasive potential and EMT phenotype of NSCLC cells. ► miR-134 regulates EMT in NSCLC cells. ► miR-134 directly targets FOXM1. ► FOXM1 is involved in TGF-β1-induced EMT in A549 cells. 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.