MiR‐370‐3p inhibits the development of human endometriosis by downregulating EDN1 expression in endometrial stromal cells
article
OA: closed
CC0
⤵ 2 in-corpus citations
AI-generated summary
MiR-370-3p, downregulated in endometriosis patients, inhibits endometrial stromal cell proliferation and invasion by targeting EDN1 expression.
One-sentence paraphrase of the abstract; not a substitute for reading it. No clinical advice. How this works
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.
My notes (saved in your browser only)
Condition tags
MeSH descriptors
Citation neighborhood
Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. [ expand to 2 hops ] — adds papers reached through this work's immediate citers/citees. Heavier; up to 60 extra dots.
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
Cited by (2)
Source provenance
- europepmc
- last seen: 2026-06-04T01:30:01.192114+00:00
- openalex
- last seen: 2026-06-04T00:00:01.174412+00:00
- pubmed
- last seen: 2026-05-13T22:24:55.077982+00:00
License: CC0
· commercial use OK