ArticleJournal of cellular and molecular medicine2022
Simvastatin inhibits stem cell proliferation in human leiomyoma via TGF-β3 and Wnt/β-Catenin pathways.
Article in Journal of cellular and molecular medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 21 citations in OpenAlex.
- Trial
- Estrogen receptor (ESR) 1 promotes uterine leiomyoma cell proliferation by enhancing mitochondrial energy metabolism via Wnt/β-catenin pathway activation.BMC women's health · 2026Article
- Review
- BMAL1 Regulates Collagen Production in the Myometrium and Leiomyomas.Reproductive sciences (Thousand Oaks, Calif.) · 2025Article
- Cholesterol and Immune Microenvironment: Path Towards Tumorigenesis.Current nutrition reports · 2024Review
- Therapeutic targeting ERRγ suppresses metastasis via extracellular matrix remodeling in small cell lung cancer.EMBO molecular medicine · 2024Article
- High glutamine increases stroke risk by inducing the endothelial-to-mesenchymal transition in moyamoya disease.MedComm · 2024Article
- Changes in Dickkopf-1, but Not Sclerostin, in Gingival Crevicular Fluid Are Associated with Peroral Statin Treatment in Patients with Periodontitis.Medicina (Kaunas, Lithuania) · 2024Article
- Review
- Article
- Update on the Role and Regulatory Mechanism of Extracellular Matrix in the Pathogenesis of Uterine Fibroids.International journal of molecular sciences · 2023Review
- Leptin induces leiomyoma cell proliferation and extracellular matrix deposition via JAK2/STAT3 and MAPK/ERK pathways.F&S science · 2022Article
- Simvastatin inhibits stem cell proliferation in human leiomyoma via TGF-β3 and Wnt/β-Catenin pathways.Journal of cellular and molecular medicine · 2022Article
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
Uterine leiomyoma (UL) is the most common gynaecologic tumour, affecting an estimated 70 to 80% of women. Leiomyomas develop from the transformation of myometrial stem cells into leiomyoma stem (or tumour-initiating) cells. These cells undergo self-renewal and differentiation to mature cells, both are necessary for the maintenance of tumour stem cell niche and tumour growth, respectively. Wnt/β-catenin and TGF-β/SMAD pathways, both overactive in UL, promote stem cell self-renewal, crosstalk between stem and mature cells, cellular proliferation, extracellular matrix (ECM) accumulation and drive overall UL growth. Recent evidence suggests that simvastatin, an antihyperlipidemic drug, may have anti-leiomyoma properties. Herein, we investigated the effects of simvastatin on UL stem cells. We isolated leiomyoma stem cells by flow cytometry using DyeCycle Violet staining and Stro-1/CD44 surface markers. We found that simvastatin inhibits proliferation and induces apoptosis in UL stem cells. In addition, it also suppressed the expression of the stemness markers Nanog, Oct4 and Sox2. Simvastatin significantly decreased the production of the key ECM proteins, collagen 1 and fibronectin. Finally, it inhibited genes and/or proteins expression of TGF-β1, 2 and 3, SMAD2, SMAD4, Wnt4, β-Catenin, LRP6, AXIN2 and Cyclin D1 in UL stem cells, all are key drivers of the TGF-β3/SMAD2 and Wnt4/β-Catenin pathways. Thus, we have identified a novel stem cell-targeting anti-leiomyoma simvastatin effect. Further studies are needed to replicate these findings in vivo.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.