MiR-370-3p inhibits the development of human endometriosis by downregulating EDN1 expression in endometrial stromal cells.

BACKGROUND: MiR-370-3p has been demonstrated to be downregulated in patients with endometriosis (EM). However, its role and molecular mechanisms in the progression of EM remain unclear.

METHODS: Real-time PCR was used to measure the expression of miR-370-3p and EDN1 in patients with or without EM. After miR-370-3p overexpression or knockdown in ectopic endometrial hEM15A cells, the changes in the proliferation, apoptosis, and migration and invasion capacities were detected by using CCK-8, flow cytometry, and transwell methods. The interplay between miR-370-3p and endothelin-1 (EDN1) was confirmed by a luciferase reporter assay.

RESULTS: Patients with EM showed adverse expression of EDN1 and miR-370-3p, especially in eutopic endometrium (EU) and ectopic endometrium (EC). MiR-370-3p inhibited the proliferation, metastasis and invasion capacities of hEM15A cells, and promoted the apoptosis. Investigation to its molecular mechanism revealed that miR-370-3p targeted EDN1 to influence biological functions of hEM15A cells.

CONCLUSION: MiR-370-3p represented as a therapeutic target for EM treatment. This article is protected by copyright. All rights reserved.