ArticleDrug design, development and therapy2019
Mifepristone inhibits IGF-1 signaling pathway in the treatment of uterine leiomyomas.
Article in Drug design, development and therapy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 17 citations in OpenAlex.
- Review
- Progesterone signaling in uterine fibroids: Molecular mechanisms and therapeutic opportunities.Life sciences · 2025Review
- Review
- The function role and synergic effect of syndecan-1 for mifepristone in uterine leiomyoma.Cytotechnology · 2021Article
- Liposomes Co-Encapsulating Cisplatin/Mifepristone Improve the Effect on Cervical Cancer: In Vitro and In Vivo Assessment.Pharmaceutics · 2020Article
- Quercetin Inhibits Adenomyosis by Attenuating Cell Proliferation, Migration and Invasion of Ectopic Endometrial Stromal Cells.Drug design, development and therapy · 2020Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeTo investigate the role of IGF-1 signaling pathway in the treatment of uterine leiomyomas with mifepristone. PATIENTS AND
methodsFrom October 2015 to December 2018, 50 patients with uterine leiomyoma were included in this study. Overexpression or siRNA of IGF-1 in primary human uterine leiomyoma cells were treated with or without mifepristone. MTT was used to evaluate cell viability in assays of cell proliferation and cytotoxicity. IGF-1 expression in the cells was measured with real-time RT-PCR and Western blotting and manipulated with lentivirus ectopic overexpression or siRNA silencing.
resultsInhibition of cell viability by mifepristone was found dependent on drug concentration and treatment time. IGF-1 and phosphorylation-ERK1/2 expression were decreased, while phosphorylation-AKT expression was increased after mifepristone treatment. IGF-1 significantly promoted cell growth, while IGF-1 knockdown and mifepristone showed synergistic inhibition effects on cell growth. The overexpression of IGF-1 reversed the inhibition of cell growth and ERK1/2 phosphorylation but showed no effect on AKT phosphorylation.
conclusionOur study for the first time demonstrated that IGF-1 signaling via ERK1/2 appears to be an important target of mifepristone in the treatment of uterine leiomyomas, which may provide a new approach to avoid leiomyoma re-growth after cessation of mifepristone.
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