MicroRNA-455-3p Inhibits Tumor Cell Proliferation and Induces Apoptosis in HCT116 Human Colon Cancer Cells
Jiantao Zheng, Zhenlv Lin, Lin Zhang, Hui Chen
(Department of Gastrointestinal Surgery, The First Affiliated Hospital of Fujian Medical University, Fuzhou, Fujian, China (mainland))
Med Sci Monit 2016; 22:4431-4437
MicroRNAs have been reported to play significant roles in pathogenesis of colorectal cancer (CRC). In the present study, we aimed to investigate the functional role of microRNA-455-3p (miR-455-3p) in CRC, as well as its underlying mechanisms.
MATERIAL AND METHODS: Human colon cancer cell line HCT116 cells were transfected with miR-455-3p mimics, inhibitors, or controls. After transfection, the effects of miR-455-3p mimics or inhibitors on cell proliferation were analyzed by 3-(4, 5-dimethyl-2- thiazolyl)-2, 5-diphenyl -2-H-tetrazolium bromide (MTT) assay and BrdU assay, and the effects of miR-455-3p mimics or inhibitors on cell apoptosis were determined. In addition, the underlying mechanisms of cell proliferation and apoptosis were explored by assessing the protein levels of cell cycle regulators and apoptosis-related protein.
RESULTS: The results showed that overexpression of miR-455-3p significantly inhibited the cell proliferation (P<0.05 or <0.01) in HCT116 cells compared with the control group, but significantly increased the apoptosis (P<0.01). On the contrary, suppression of miR-455-3p significantly increased the cell proliferation but decreased the apoptosis. Moreover, we found that overexpression of miR-455-3p significantly elevated the protein levels of p27 kinase inhibition protein (KIP) 1, Bax, pro-caspase-3, and active caspase-3, and markedly downregulated the levels of B-cell lymphoma-2 (Bcl-2). Contrary results were found by suppression of miR-455-3p. However, there were no significant differences in p21 expression.
CONCLUSIONS: MiRNA-455-3p functions as an anti-oncogene in HCT116 cells by inhibiting cell proliferation and inducing of apoptosis.
Keywords: Cell Proliferation - genetics, Cell Line, Tumor, Apoptosis - genetics, Colonic Neoplasms - therapy, Down-Regulation, Genes, Tumor Suppressor, HCT116 Cells, Humans, MicroRNAs - metabolism, Signal Transduction