ArticleIranian journal of biotechnology2025
MiR-27a-3p Enhances Endometrial Cancer Growth and EMT by Targeting LIFR and Activating the p38/MAPK Pathways.
Article in Iranian journal of biotechnology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: 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. Objectives: The purpose of this study was to investigate the function and mechanism of miR-27a-3p in the growth and EMT of EC. Materials and Methods: 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. Results: 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. Conclusion: 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.
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