MiR-27a-3p Enhances Endometrial Cancer Growth and EMT by Targeting LIFR and Activating the p38/MAPK Pathways.

MiR-27a-3p was linked to the growth, progression, and metastasis of many cancers; however, its role in endometrial cancer (EC) and the related mechanisms has not received as much research. Leukemia inhibitory factor receptor (LIFR) has been considered a prognostic and immune biomarker for EC. This work sought to determine if miR-27a-3p regulates LIFR in the malignant development of EC cells and to investigate the signaling pathways involved. The purpose of this study was to investigate the function and mechanism of miR-27a-3p in the growth and EMT of EC. The TCGA database predicted the expression levels of miR-27a-3p and LIFR in the EC. The target Scan database, along with the dual luciferase experiment, confirmed the targeting link between miR-27a-3p and LIFR. The levels of miR-27a-3p and LIFR in normal human endometrial cells EEC and EC cells were identified using RT-qPCR and Western blot tests. After interfering with miR-27a-3p or LIFR level, EC cell proliferation, migration, and invasion capacities, as well as the expression levels of proteins involved in EMT and the p38/MAPK signaling pathways were examined to investigate the intrinsic mechanism of miR-27a-3p regulation of EC. In EC cells, miR-27a-3p and LIFR were dramatically increased and decreased, respectively. miR-27a-3p targeting inhibited LIFR, further interfering with the p38/MAPK signaling pathway. Knocking down miR-27a-3p or overexpressing LIFR were efficient in suppressing the malignant biological characteristics and EMT of EC cells. Adding a p38/MAPK signaling pathway inhibitor partially decreases the influence of miR-27a-3p or LIFR on EC cells. MiR-27a-3p activates the p38/MAPK signaling pathway by targeting LIFR down-regulation, promoting malignant biological behavior and EC cell EMT. This pathway may give ideas for EC clinical treatment.