MiR‐370‐3p inhibits the development of human endometriosis by downregulating EDN1 expression in endometrial stromal cells
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MiR-370-3p, downregulated in endometriosis patients, inhibits endometrial stromal cell proliferation and invasion by targeting EDN1 expression.
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Abstract
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.
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References (27)
- Bradykinin system is involved in endometriosis‐related pain through endothelin‐1 production via openalex
- Differentially-Expressed miRNAs in Ectopic Stromal Cells Contribute to Endometriosis Development: The Plausible Role of miR-139-5p and miR-375 via openalex
- High-throughput mRNA sequencing of stromal cells from endometriomas and endometrium via openalex
- Immunoreactive endothelin-1 concentrations in follicular fluid of women with and without endometriosis undergoing in vitro fertilization-embryo transfer via openalex
- Implications of immune dysfunction on endometriosis associated infertility via openalex
- Increased circulating miR-370-3p regulates steroidogenic factor 1 in endometriosis via openalex
- MicroRNA expression profiling in endometriosis-associated infertility and its relationship with endometrial receptivity evaluated by ultrasound via openalex
- MicroRNAs and Endometriosis: Distinguishing Drivers from Passengers in Disease Pathogenesis via openalex
- miR-191 Modulates Malignant Transformation of Endometriosis Through Regulating TIMP3 via openalex
- miR-200c suppresses endometriosis by targeting MALAT1 in vitro and in vivo via openalex
- Regulation of miR-33b on endometriosis and expression of related factors. via openalex
- Regulation of miR-33b on endometriosis and expression of related factors. via openalex
- Update on endometriosis pathogenesis via openalex
- ZEB1 expression is a potential indicator of invasive endometriosis via openalex
- W2799524602 via openalex
- W2901616594 via openalex
- W2038362499 via openalex
- W2035301529 via openalex
- W2983394721 via openalex
- W2989977962 via openalex
- W4247544731 via openalex
- W6736467252 via openalex
- W6751069829 via openalex
- W7073878945 via openalex
- W2548567961 via openalex
- W2344056558 via openalex
- W2783998471 via openalex
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