MicroRNAs (miRNAs) have been implied to play crucial roles for epithelial-to-mesenchymal transition (EMT) of non-small-cell lung cancer cells (NSCLC cells). Here we found that the expression of miR-149, downregulated in lung cancer, was inversely correlated with invasive capability and the EMT phenotype of NSCLC cells. miR-149 inhibited EMT in NSCLC cells. Furthermore, we demonstrated that miR-149 directly targeted Forkhead box M1 (FOXM1), and FOXM1 was involved in the EMT induced by TGF-β1 in A549 cells. Overexpression of FOXM1 restored EMT process inhibited by miR-149. Our work suggested that miR-149 might be an EMT suppressor in NSCLC cells. 1. Introduction Lung cancer was the most frequently occurring malignant cancer, and the leading death cause of lung cancer was metastasis. Tumor metastasis involved several steps including separation, migration, invasion, and formation of a new tumor nodule. Epithelial-to-mesenchymal transition (EMT) played key role in the process of cancer metastasis [1]. EMT not only changed cell morphology but also induced cells to acquire essential new functions like migration and invasion. EMT was characterized by different regulations of epithelial and mesenchymal genes. The increase of mesenchymal markers vimentin and N-cadherin and the loss of epithelial marker E-cadherin were associated with EMT [2, 3]. Transforming growth factor-β1 (TGF-β1) had been suggested to be an important inducer of EMT in various cancers [4]. MicroRNAs (miRNAs) were a class of small noncoding RNAs, ~18–25 nucleotides, which regulated gene expression posttranscriptionally via inhibiting translation or inducing target mRNA degradation. Dysregulation of miRNAs occurred in a variety of cancers, and several miRNAs acted as essential modulators for EMT in non-small-cell lung cancer (NSCLC). Previous studies reported a downregulation of miR-149 in NSCLC, and miR-149 functioned as a tumor suppressor in human glioma and gastric cancer [5–7]. However, the role of miR-149 in the EMT of NSCLC cells remained poorly understood. In the present study, we found that miR-149 was significantly downregulated and the expression of miR-149 was inversely correlated with the invasive capability and EMT phenotype of NSCLC cells. Ectopic expression of miR-149 inhibited EMT in NSCLC cells. Furthermore, we found that miR-149 directly targeted FOXM1, a potential metastasis promoter. 2. Materials and Methods 2.1. Cell Lines Four NSCLC cell lines including A549, Calu3, Calu1, and H1299 were obtained from ATCC. These cells were grown in RPMI 1640 media (Whitaker Biomedical
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