MicroRNA-132 inhibits migration, invasion and epithelial-mesenchymal transition by regulating TGFβ1/Smad2 in human non-small cell lung cancer

OBJECTIVES: Increasing evidence shows that microRNA involves in the development of several types of cancers, however, the role of microRNA-132 (miR-132) in non-small cell lung cancer (NSCLC) metastasis remains largely unknown. In this study, we aimed to investigate the effect of miR-132 on the epithelial-mesenchymal transition (EMT) and the potential mechanisms in NSCLC. PATIENTS AND METHODS: The Quantitative real-time PCR (QRT-PCR) was used to detect the miR-132 levels in 15 NSCLC tissues and cell lines. Transwell and wound healing assays were used to evaluate the function of miR-132 in NSCLC cell metastasis. EMT-related markers were determined by using qRT-PCR. EMT-related TGF beta 1/Smad2 signaling pathway was explored using Western blot. RESULTS: MiR-132 expression level was lower in NSCLC tissues compared with the matched adjacent normal tissues. It was also downregulated in A549 cell lines compared to normal lung epithelial cell BEAS-2B. MiR-132 overexpression obviously inhibited migration and invasion capacities in A549 cells while miR-132 down-regulation would enhance such capacities. Expression of EMT-related markers and TGF beta 1/Smad2 was higher in A549 cells transfected with miR-132 inhibitor compared with those transfected with miR-132 mimic. Moreover, expression of EMT-related markers and Smad2 was increased in NSCLC tissues compared to in the adjacent normal tissues and the reverse expression of miR-132 and Smad2 was observed. CONCLUSIONS: These results indicate that miR-132 may play a suppressive role in the metastasis of NSCLC cells by promoting EMT via TGF beta 1/Smad2 signaling pathway.