ArticleCarcinogenesis2015
17β-estradiol inhibits spreading of metastatic cells from granulosa cell tumors through a non-genomic mechanism involving GPER1.
Article in Carcinogenesis, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 27 citations in OpenAlex.
- Granulosa cell tumors and menopausal hormone therapy: A narrative review.Gynecologic oncology reports · 2026Review
- Article
- Enhancing the preoperative diagnostic accuracy for ovarian sex cord-stromal tumors through evaluation of clinical and imaging characteristics.Quantitative imaging in medicine and surgery · 2025Article
- Implications of estrogen and its receptors in colorectal carcinoma.Cancer medicine · 2023Review
- Melatonin Signaling Pathways Implicated in Metabolic Processes in Human Granulosa Cells (KGN).International journal of molecular sciences · 2022Article
- Estradiol Signaling at the Heart of Folliculogenesis: Its Potential Deregulation in Human Ovarian Pathologies.International journal of molecular sciences · 2022Review
- Clinical and paraclinical features, outcome, and prognosis of ovarian granulosa cell tumor: A retrospective study of 28 Vietnamese women.Rare tumors · 2022Article
- The impact of G protein-coupled oestrogen receptor 1 on male breast cancer: a retrospective analysis.Contemporary oncology (Poznan, Poland) · 2021Article
- Review
- Functional Profiling of FSH and Estradiol in Ovarian Granulosa Cell Tumors.Journal of the Endocrine Society · 2020Article
- Article
- New Drug Repositioning Candidates for T-ALL IdentifiedFrontiers in oncology · 2020Article
- Apelin abrogates the stimulatory effects of 17β-estradiol and insulin-like growth factor-1 on proliferation of epithelial and granulosa ovarian cancer cell lines via crosstalk between APLNR and ERα/IGF1R.Molecular biology reports · 2019Article
- G protein-coupled estrogen receptor in colon function, immune regulation and carcinogenesis.World journal of gastroenterology · 2019Review
- Comparative Tumorigenicity and DNA Damage Induced by Dibenzo[ def,p]chrysene and Its Metabolites in the Mouse Ovary.Chemical research in toxicology · 2018Article
Corrections and comments
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Authors and funding
10 authors at 7 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Granulosa cell tumor (GCT) is a rare and severe form of sex-cord stromal ovarian tumor that is characterized by its long natural history and tendency to recur years after surgical ablation. Because there is no efficient curative treatment beyond surgery, ~20% of patients die of the consequences of their tumor. However, very little is known of the molecular etiology of this pathology. About 70% of GCT patients present with elevated circulating estradiol (E2). Because this hormone is known to increase tumor growth and progression in a number of cancers, we investigated the possible role of E2 in GCTs. Cell-based studies with human GCT metastases and primary tumor-derived cells, ie KGN and COV434 cells, respectively, aimed at evaluating E2 effect on cell growth, migration and invasion. Importantly, we found that E2 did not affect GCT cell growth, but that it significantly decreased the migration and matrix invasion of metastatic GCT cells. Noteworthy, our molecular studies revealed that this effect was accompanied by the inhibition through non-genomic mechanisms of extracellular signal-regulated kinase 1/2 (ERK1/2), which is constitutively activated in GCTs. By using pharmacological and RNA silencing approaches, we found that E2 action was mediated by G protein-coupled estrogen receptor 1 (GPER1) signaling pathway. Analyses of GPER1 expression on tissue microarrays from human GCTs confirmed its expression in ~90% of GCTs. Overall, our study reveals that E2 would act via non-classical pathways to prevent metastasis spreading in GCTs and also reveals GPER1 as a possible target in this disease.
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