miR-769-5p inhibits cellular behaviors associated with endometriosis progression by directly targeting follistatin in vitro

The pathogenesis of endometriosis (EM) remains intricate and multifactorial. This study aimed to investigate the biological functions of microRNA-769-5p (miR-769-5p) in an in vitro model of EM. Serum was obtained from 120 EM patients and 100 healthy controls. miRNA and mRNA expression were quantified by RT-qPCR. Functional analyses of miR-769-5p were performed in vitrousing cell counting kit-8 (CCK-8) cell proliferation assays, Transwell assays, and dual-luciferase assays in an endometriosis-derived stromal cell line (hEM15A). miR-769-5p was markedly down-regulated in EM sera and correlated inversely with disease severity (p < 0.001). Moreover, miR-769-5p exhibited high diagnostic accuracy for EM (AUC = 0.9166, p < 0.001). In the hEM15A cell model, overexpression of miR-769-5p effectively suppressed the proliferation, migration, and invasion capabilities of EM-derived stromal cells (p < 0.001). miR-769-5p targeted follistatin (FST) and negatively regulated its expression in vitro (p < 0.001). In contrast, FST overexpression could partially reverse the inhibitory effects of miR-769-5p-mimic on these EM-derived cells. Our findings indicate that miR-769-5p is downregulated in EM serum. Furthermore, in vitro experiments suggest that it can target FST to inhibit proliferation, migration, and invasion of ectopic endometrial stromal cells.