MIR-203A-5P SUPPRESSES CERVICAL CANCER CELL TUMORIGENESIS AND EMT VIA TARGETING MAPK1

Introduction: Cervical cancer (CC) is the fourth most prevalent malignancy worldwide. CC is usually asymptomatic in initial stage, if the treatment is not timely, it can be life-threatening. MiR-203 was downregulated in CC tissues, and a potential biomarker for the early stages of CC. In this study, the role and underlying mechanisms of miR-203a-5p in CC cells were investigated. Case report. The expressions of miR-203a-5p and mitogen-activated protein kinase 1 (MAPK1) in CC tissue and cells were measured by real time reverse transcription polymerase chain reaction (RT-qPCR). The protein levels of MAPK1 and epithelial to mesenchynzal transition (EMT)-related proteins (E-cadherin, N-cadherin, Vimentin and Snail) in CC cells were detected by western blot assay. The effects of miR-203a-5p and MAPK1 on proliferation, migration, invasion and apoptosis were analyzed by cell counting kit-8 (CCK-8), transwell and flow cytometry assays, respectively. MiR-203a-5p-MAPKI binding interaction was predicted and demonstrated by Targetscan and dual luciferase reporter assays, respectively. MiR-203a-5p was downregulated, and MAPK1 was upregulated in CC tissues and cells. MiR-203a-5p suppressed proliferation, migration, invasion, and induced apoptosis of CC cells. MiR-203a-5p elevated the protein level of E-cadherin and attenuated the protein levels N-cadherin, Vimentin and Snail in CC cells. MAPK1 was demonstrated as a target of miR-203a-5p. MiR-203a-5p retarded proliferation, migration, invasion, EMT, and boosted apoptosis of CC cells through targeting MAPK1. Conclusion: MiR-203a-5p could suppress CC cell proliferation, migration, invasion, EMT and boosted apoptosis by regulating MAPK1 expression, hinting that miR-203a-5p is a potential prognostic biomarker and therapeutic target for CC.