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MiR‐370‐3p inhibits the development of human endometriosis by downregulating EDN1 expression in endometrial stromal cells
Author(s) -
Zhou Shun,
Huang Chengyi,
Wang Wei,
Liu Juan
Publication year - 2021
Publication title -
cell biology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 77
eISSN - 1095-8355
pISSN - 1065-6995
DOI - 10.1002/cbin.11552
Subject(s) - gene knockdown , flow cytometry , stromal cell , endometriosis , apoptosis , cancer research , ectopic expression , luciferase , reporter gene , chemistry , cell growth , biology , microbiology and biotechnology , medicine , gene expression , transfection , gene , biochemistry
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. Real‐time polymerase chain reaction was used to measure the expression of miR‐370‐3p and endothelin‐1 (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 cell counting kit‐8, flow cytometry, and transwell methods. The interplay between miR‐370‐3p and EDN1 was confirmed by a luciferase reporter assay. Patients with EM showed adverse expression of EDN1 and miR‐370‐3p, especially in eutopic endometrium and ectopic endometrium. MiR‐370‐3p inhibited the proliferation, metastasis, and invasion capacities of hEM15A cells and promoted apoptosis. Investigation of its molecular mechanism revealed that miR‐370‐3p targeted EDN1 to influence the biological functions of hEM15A cells. MiR‐370‐3p represented as a therapeutic target for EM treatment.