title: 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‑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.
authors.affiliation: Department of Oral Pathology, School of Dentistry, Institute                     of Oral Bioscience, Chonbuk National University, Jeonju, Republic of Korea.
authors.forename: Ji-Ae
authors.initials: JA
authors.lastname: Shin
authors.forename: Chengming
authors.initials: C
authors.lastname: Li
authors.forename: Eun-Sun
authors.initials: ES
authors.lastname: Choi
authors.forename: Sung-Dae
authors.initials: SD
authors.lastname: Cho
authors.forename: Nam-Pyo
authors.initials: NP
authors.lastname: Cho
mesh_terms: D000818:Animals; D018277:Carcinoma, Mucoepidermoid / Q000378:metabolism / Q000473:pathology; D049109:Cell Proliferation / Q000187:drug effects; D002471:Cell Transformation, Neoplastic / Q000187:drug effects; D002478:Cells, Cultured; D050759:Cyclin-Dependent Kinase Inhibitor p21 / Q000378:metabolism; D050760:Cyclin-Dependent Kinase Inhibitor p27 / Q000378:metabolism; D005347:Fibroblasts / Q000166:cytology / Q000187:drug effects; D059585:G1 Phase Cell Cycle Checkpoints / Q000187:drug effects; D006801:Humans; D051379:Mice; D035683:MicroRNAs / Q000235:genetics / Q000378:metabolism* / Q000494:pharmacology; D059807:S Phase Cell Cycle Checkpoints / Q000187:drug effects; D012468:Salivary Gland Neoplasms / Q000378:metabolism / Q000473:pathology; D016329:Sp1 Transcription Factor / Q000378:metabolism; D013755:Tetradecanoylphorbol Acetate / Q000633:toxicity; D014162:Transfection
chemical_list: D050759:Cyclin-Dependent Kinase Inhibitor p21; C547276:MIRN127 microRNA, human; D035683:MicroRNAs; D016329:Sp1 Transcription Factor; D050760:Cyclin-Dependent Kinase Inhibitor p27; D013755:Tetradecanoylphorbol Acetate