High expression of microRNA-127 is involved in cell cycle arrest in MC-3 mucoepidermoid carcinoma cells

Abstract

microRNAs (miRs) are small endogenous non-coding RNAs and are associated with the pathogenesis of a number of types of human cancer. However, miR-127-3p in mucoepidermoid carcinoma (MEC) has not been studied. The present study aimed to analyze the importance of miR-127-3p in MC-3 human MEC cells. Analyses of the growth inhibitory effect and the associated mechanism of miR-127-3p were performed using 3-(4,5-dimethylthiazol-20yl)-(3-carboxy-methoxyphenyl)-2-(4-sulphophenyl)-2H-tetrazolium assay, flow cytometry, 4'-6-diamidino-2-phenylindole staining, anchorage-independent cell transformation assay and western blot analysis. Transfection of exogenous miR-127-3p into MC-3 cells inhibited cell viability and led to G(1)/S cell cycle arrest. In addition, miR-127-3p also decreased neoplastic cell transformation in TPA-induced JB6 mouse epidermal and MC-3 cells. In addition, miR-127-3p decreased specificity protein 1 (Sp1) expression and increased p21 and p27 expression which are Sp1-dependent cell cycle-related proteins. However, miR-127-3p did not induce apoptosis or affect expression levels of myeloid cell leukemia-1 or survivin. miR-127-3p induced G(1)/S cell cycle arrest and increased p21 and p27 expression via modulation of Sp1. Therefore, miR-127-3p may be a therapeutic target for human MEC.