06 May 2016 : Laboratory Research
MicroRNA-340 Inhibits Tumor Cell Proliferation and Induces Apoptosis in Endometrial Carcinoma Cell Line RL 95-2Wei XieBCDEF, Wen QinBCDEF, Yalin KangCDF, Ziyan ZhouCD, Aiping QinADEFG
Med Sci Monit 2016; 22:1540-1546
BACKGROUND: The purpose of our study was to investigate the functional role of microRNA-340 (miR-340) in endometrial carcinoma (EC).
MATERIAL AND METHODS: Human EC cell line RL 95-2 was transfected with miR-340 mimics, inhibitors, or controls. After 48 h of transfection, the cell viability was determined by 3-(4, 5-dimethyl-2- thiazolyl)-2, 5-diphenyl -2-H-tetrazolium bromide (MTT) assay. The BrdU assay and apoptosis assay were performed to determine the effects of miR-340 mimics or inhibitors on cell proliferation and apoptosis, respectively. The underlying mechanisms involved in cell proliferation and apoptosis were explored by measuring the protein levels of cell cycle regulators (p27 kinase inhibition protein (KIP) 1 and p21) and apoptosis-related factors (B-cell lymphoma-2 (Bcl-2), Bax, pro-Caspase 3, and active-Caspase-3).
RESULTS: Overexpression of miR-340 significantly inhibited the cell viability (P<0.05) and cell proliferation (P<0.01) of RL 95-2 cells compared with the control group, but increased the apoptosis (P<0.01). However, suppression of miR-340 had opposite results. Moreover, the protein levels of p27 KIP1, Bax, pro-Caspase 3, and active-Caspase-3 were significantly increased by overexpression of miR-340 but were statistically decreased by suppression of miR-340. Contrary results were found in the protein levels of Bcl-2. However, no significant differences were found in p21 expression.
CONCLUSIONS: MiRNA-340 acts as an anti-oncogene in EC cell line RL 95-2 by inhibition of tumor cell proliferation and induction of apoptosis.
Keywords: Caspase 3 - metabolism, Cell Line, Tumor, Cell Survival - genetics, Cyclin-Dependent Kinase Inhibitor p27 - metabolism, Endometrial Neoplasms - pathology, MicroRNAs - metabolism, bcl-2-Associated X Protein - metabolism
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