Mir-543 Inhibits The Migration And Epithelial-To-Mesenchymal Transition Of Tgf-Beta-Treated Endometrial Stromal Cells Via The Mapk And Wnt/Beta-Catenin Signaling Pathways

Intrauterine adhesion (IUA) is one of the most prevalent reproductive system diseases in females. MicroRNAs (miRNAs) are reported to be master regulators in a variety of diseases, including IUA, but the role of microRNA-543 (miR-543) in IUA remains to be elucidated. In this study, we observed that miR-543 was downregulated in transforming growth factor-beta (TGF-beta)-treated endometrial stromal cells (ESCs). Functionally, we observed that miR-543 suppressed the migration, epithelial-to-mesenchymal transition (EMT), and inhibited expression of extracellular matrix (ECM) proteins in TGF-beta-treated ESCs. Mechanistically, MAPK1 is targeted by miR-543 after prediction and screening. A luciferase reporter assay demonstrated that miR-543 complementarily binds with the 3' untranslated region of mitogen-activated protein kinase 1 (MAPK1), and western blot analysis indicated that miR-543 negatively regulates MAPK1 protein levels. In addition, results from rescue assays showed that miR-543 inhibits the migration and EMT of TGF-beta-treated ESCs by targeting MAPK1. In addition, we observed that miR-543 inactivates the Wnt/beta-catenin signaling pathway through inhibiting the phosphorylation of MAPK1 and beta-catenin. Finally, we confirmed that miR-543 represses migration, EMT and inhibits levels of ECM proteins in TGF-beta-treated ESCs by targeting the Wnt/beta-catenin signaling pathway. Our results demonstrated that miR-543 suppresses migration and EMT of TGF-beta-treated ESCs by targeting the MAPK and Wnt/beta-catenin pathways.