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

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‑carboxymethoxyphenyl)‑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 G1/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 G1/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.