RESUMEN
@# Objective: To investigate the effects and mechanisms of miR-129-5p on invasion, migration and epithelial-mesenchymal transition (EMT) of cervical cancer HeLa cells. Methods:Cervical cancer HeLa cells were selected. The target gene of miR-129-5p was screened by bioinformatics prediction software, and the targeting relationship between miR-129-5p and MAPK1 was verified by dual luciferase reporter gene assay. HeLa cells were transfected with miR-129-5p mimic, miR-129-5p inhibitor and pcDNA-MAPK1 alone or in combination.The expressions of miR-129-5p and MAPK1 in HeLa cells were detected by qPCR; the invasion and migration ability of HeLa cells were detected by Transwell and scratch-healing experiments, respectively; and the expressions of E-cadherin, N-cadherin, MAPK1, STAT3 and Bcl-xL were detected by WB. The subcutaneous xenograft model of HeLa cells in nude mice was constructed to observe the effect of miR-129-5p over-expression on the growth of transplanted tumors. The expressions of EMT and MAPK1 pathwayrelated proteins in transplanted tumor tissues were detected by WB. Results: miR-129-5p could bind with the 3'UTR region of MAPK1, and over-expression of miR-129-5p targetedly inhibited the expression of MAPK1 (P<0.01). Compared with the control group, the number of invasive cells in the miR-129-5p mimic group decreased (P<0.01), the scratch healing rate decreased (all P<0.01); The expression of E-cadherin was up-regulated, and the expressions of N-cadherin, MAPK1, STAT3 and Bcl-xL were down-regulated (all P< 0.01), while co-transfection of MAPK1 reversed the above phenomenon.The nude mice HeLa cell xenograft model was successfully established. Compared with the control group, the tumor mass of the miR-128-3p mimic group was reduced; the expression of E-cadherin was up-regulated in tumor tissues, while the expressions of N-cadherin, MAPK1, STAT3 and Bcl-xL were down-regulated (all P<0.01). Conclusion: Over-expression of miR-129-5p inhibits invasion, migration and epithelial-mesenchymal transition of cervical cancer HeLa cells by targeting MAPK1.