Role of miR-34c downregulated by EBV in promoting proliferation and migration of nasopharyngeal carcinoma cells and its mechanism

ObjectiveTo investigate the role of miR-34c downregulated by Epstein-Barr virus (EBV) in promoting the proliferation, migration, and invasion of nasopharyngeal carcinoma cells and its mechanism.

MethodsThe expression level of miR-34c in EBV-negative nasopharyngeal carcinoma SUNE1, CNE2, HK1 cells, and EBV-positive C666-1 cells was detected by qPCR.MiR-34c mimics were constructed to analyze the influence of miR-34c on the biological function of nasopharyngeal carcinoma cells.CCK-8, scratch healing assay, and Transwell cell invasion assay were applied to detect the proliferation, migration, and invasion ability of nasopharyngeal carcinoma cells.Western blotting was employed to determine the expression levels of migration and invasion-related proteins, and Erk1/2 signaling pathway proteins in cells.

ResultsMiR-34c was downregulated in EBV-positive C666-1 cells (P < 0.05).CCK-8 results showed that the viability of C666-1 cells in the miR-34c group was significantly lower than that in the EBV group at 16, 24, and 48 hours (P < 0.01).The scratch assay and Transwell assay results indicated that compared with the miR-34c group, the migration and invasion ability of C666-1 cells in the EBV group were significantly enhanced (P < 0.01).Western blotting results showed that compared with the miR-34c group, the expression of migration and invasion-related proteins Vimentin, Snail, MMP-2, MMP-3, and Erk1 and Erk2 proteins of C666-1 cells in the EBV group were significantly increased (P < 0.01).

ConclusionsMiR-34c is downregulated in EBV-positive nasopharyngeal carcinoma cells, and miR-34c downregulated by EBV can enhance the proliferation, invasion, and migration capacities of nasopharyngeal carcinoma cells and activate the Erk1/2 signaling pathway.