Background Endometriosis (EMs) seriously affects women's health, and its pathogenesis is still unknow. miR-363-3p is a recently identified tumor suppressor in a variety of cancers, and its effect on EMs pathogenesis has not been elucidated.

Objective To analyze the effects of miR-363-3p on the proliferation and apoptosis of endometrial stromal cells (EnSCs) and to explore its possible underlying mechanisms.

Methods In vitro culture of EnSCs derived from the eutopic endometrium of EMs patients was conducted. The binding ability between miR-363-3p and methionine sulfoxide reductase B3 (MsrB3) was detected using luciferase reporter assay. A miR-363-3p overexpression model was constructed via liposome transfection, and the cells were divided into miR-363-3p overexpression group, miR-NC control group, and miR-363-3p + MsrB3 co-transfection group. Changes in MsrB3 protein expression among the three groups were examined by Western blot. The proliferation and apoptosis capabilities of the three groups were assessed using CCK-8 assay and flow cytometry, respectively.

Results The dual-luciferase reporter assay confirmed that miR-363-3p could bind to MsrB3 (P < 0.001). Overexpression of miR-363-3p suppressed the protein expression level of MsrB3, but showed no significant effect on the mRNA expression of MsrB3 (P > 0.05). Overexpression of miR-363-3p resulted in decreased proliferative capacity (P < 0.01) and increased apoptotic rate (P < 0.01) of EnSCs. Furthermore, overexpression of MsrB3 reversed the miR-363-3p-induced reduction in cell proliferation (P < 0.01) and elevation in apoptosis rate (P < 0.01).

Conclusion MsrB3 is a target gene of miR-363-3p, which may reduce the viability of endometrial stromal cells by downregulating MsrB3 expression.