Regulation and mechanism of miR-1 overexpression on nasopharyngeal carcinoma cells

ZHANG Kai; WANG Jianhong; LUO Xiaozou

doi:10.3969/j.issn.1002-266X.2018.48.005

Abstract：Objective To investigate the regulatory effect and mechanism of microRNA-1 overexpression on nasopharyngeal carcinoma cell line (CNE2).Methods CNE2 cells were randomly divided into the control group and transfection group, which were transfected with negative control microRNA mimics and microRNA-1 mimimics, respectively.CCK8 assay was used to detect the proliferation of CNE2 cells, flow cytometry was used to detect the growth cycle of CNE2 cells, Scratch assay was used to detect the migration ability of CNE2 cells, Transwell assay was used to detect the invasion ability of CNE2 cells, qRT-PCR and Western blotting were used to detect the effect of microRNA-1 on the mRNA and protein expression of c-met gene.We used microRNA target gene database to predict whether c-met was one of the potential targets of microRNA-1.Luciferase reporter gene assay was used to detect whether microRNA-1 could bind to 3'-UTR of c-met.Results The cell proliferation, migration and invasion abilities of the transfection group were lower than those of the control group (all P＜0.05).Compared with the control group, the proportion of cells in the G0/G1 phase was higher, while the proportion of cells in the S phase was lower (P＜0.05), and there was no significant difference in the proportion of cells in the G2phase (P>0.05).Compared with the control group, the mRNA and protein expression of c-met gene in the transfection group was lower (P＜0.05).Mir-1 mimics significantly inhibited the luciferase activity of wild-type plasmid c-met, but had no significant effect on the luciferase activity of mutant plasmid c-met.Conclusion Overexpression of microRNA-1 can inhibit the proliferation, migration and invasion of nasopharyngeal carcinoma cells, and its mechanism may be related to the reduction of the expression of c-met in cells.