MicroRNA-639 regulates epithelial-mesenchymal transition of tongue squamous carcinoma

Objective To investigate the regulatory function of miR-639 on the epithelial-mesenchymal transition in tongue squamous carcinoma. Methods SCC9 TGF-β1 and CAL27 TGF-β1 were obtained by treating SCC9 and CAL27 with human recombinant TGF-β1. Expressions of EMT markers E-cadherin, Vimentin, were determined by quantitative real-time PCR and western blotting. MicroRNA microarray was used to demonstrate the differentially expressed miRNA and quantitative real-time PCR were used to verify their expressions. We disturbed expressions of miR-639 and investigated effects on epithelial-mesenchymal features, invasiveness and motility of TSCC cells. Results Transfection of the TGF-β1 induced TSCC cells with miR-639 mimics, but not the non-relevant miRNA mimics specifically increased miR-639 level. Reduction of miR-639 improved the ability of invasion and migration (P < 0.05) , induced EMT in TSCC cells. Ectopic expression of miR-639 surpressed the ability of invasion, migration (P < 0.05) and reversed the mesenchymal features in TSCC cells. Conclusions MiR-639 mimics could regulate EMT in TSCC cells. Transfection of the TGF-β1 induced TSCC cells with miR-639 mimics could reverse the mesenchymal features and surpress the ability of invasion and migration in TSCC cells. Key words: MicroRNA-639; Transforming growth factor-β1; Epithelial-mesenchymal transition; Neoplasms, squamous cell; Tongue neoplasms