Study on the role of miR-146b-3p in the occurrence and development of endometriosis

Objectives A chronic inflammatory disease, endometriosis is recognized by the ectopic tissue growth of endometrium, but its pathogenesis has not been fully elucidated. Recently, miRNAs have been identified as a key regulator in the pathological process of endometriosis. This study investigated the function and molecular mechanism of miR-146b-3p in the occurrence and development of endometriosis. Methods In this study, 90 patients with endometriosis and 90 age-matched patients who had surgery for uterine fibroids or simple ovarian cysts were selected for the research objects. miR-146b-3p and UNC5C levels were examined by qRT-PCR in clinical endometriotic tissues and normal tissues. The impact of miR-146b-3p on endometriotic cells was verified through transfection of miR-146b-3p mimic or inhibitor. Apoptosis and proliferation were detected using flow cytometry and CCK8 assay. Transwell method was employed for examination of cell migration and invasion. The interaction of miR-146b-3p and UNC5C was detected via luciferase activity. Results miR-146b-3p levels were significantly elevated in endometriotic tissues and gradually raised with increasing rASRM grade. In endometriotic cells, up-regulation of miR-146b-3p inhibited apoptosis, facilitated cell proliferation, migration and invasion, and elevated IL-6 and TNF-α, whereas downregulation of miR-146b-3p exhibited opposite trend. In addition, miR-146b-3p targeted UNC5C, which altered the influences of miR-146b-3p on apoptosis, proliferation, migration, invasion, and inflammatory responses. Conclusions This study found that miR-146b-3p regulates inflammatory response and progression of endometriosis by targeting UNC5C, which provided a theoretical basis for the exploitation of new diagnostic biomarkers or searching for potential therapeutic targets.