Abstract: Objective To investigate the effect and mechanism of miR-26b on the migration and epithelial mesenchymal transition of cervical cancer cells. Methods miR-26b mimic was transfected into C33A cervical cancer cells by liposome-mediated method. The experiment was divided into negative control group, scramble control group and miR-26b mimic group. The expression of miR-26b and its target genes mRNA were detected by real-time fluorescence quantitative PCR. The cell migration ability was examined by scratch-wound assay. The expression of E-cadherin and N-cadherin proteins were detected by Western blot. Dual luciferase gene reporter assays were used to examine whether miR-26b regulates the expression of Smad4. Results Compared with normal cervical epithelial cells, expression levels of miR-26b mRNA were all lower in SiHa, HeLa, Caski and C33A cells, among which C33A cells were the most obvious. mRNA expression levels of miR-26b were significantly increased in C33A cells by transfection of miR-26b mimic. Over-expression of miR-26b can significantly inhibit the migration of C33A cells, increase the expression of E-cadherin protein and reduce the expression of N-cadherin protein, and inhibit the process of epithelial mesenchymal transition. The potential target genes of miR-26b were predicted by TargetScan, PicTar and miRDB software. Based on the annotated functions for these genes, CXCL14, Smad4, TRAF5 and EphA2 were speculated to be the major potential target genes of miR-26b. Dual luciferase gene reporter assays confirmed that miR-26b can directly regulate the expression of Smad4. Conclusions miR-26b may inhibit the migration of cervical cancer cells and the process of epithelial mesenchymal transition by regulating the expression of Smad4.

Key words: microRNA-26b, cervical cancer, C33A cells, migration, epithelial mesenchymal transition