ArticleMolecular and cellular endocrinology2013
Granulosa cell tumor mutant FOXL2C134W suppresses GDF-9 and activin A-induced follistatin transcription in primary granulosa cells.
Article in Molecular and cellular endocrinology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 22 citations in OpenAlex.
- Whole transcriptome sequencing reveals the functional regulation of chicken reproduction by lncRNAs, miRNAs, and mRNAs across the hypothalamus-pituitary-ovary axis.Frontiers in veterinary science · 2025Article
- Uncovering Tumor-Promoting Roles of Activin A in Pancreatic Ductal Adenocarcinoma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Immunohistochemical markers of prognosis in adult granulosa cell tumors of the ovary - a review.Journal of ovarian research · 2023Review
- FOXO1 mitigates the SMAD3/FOXL2Journal of translational medicine · 2021Article
- FOXO1 Negates the Cooperative Action of FOXL2Journal of the Endocrine Society · 2019Article
- First-in-Human Phase I Study of the Activin A Inhibitor, STM 434, in Patients with Granulosa Cell Ovarian Cancer and Other Advanced Solid Tumors.Clinical cancer research : an official journal of the American Association for Cancer Research · 2019Article
- FOXL2C134W-Induced CYP19 Expression via Cooperation With SMAD3 in HGrC1 Cells.Endocrinology · 2018Article
- Uterine Foxl2 regulates the adherence of the Trophectoderm cells to the endometrial epithelium.Reproductive biology and endocrinology : RB&E · 2018Article
- The molecular mechanism of ovarian granulosa cell tumors.Journal of ovarian research · 2018Review
- Article
- Roles of binding elements, FOXL2 domains, and interactions with cJUN and SMADs in regulation of FSHβ.Molecular endocrinology (Baltimore, Md.) · 2014Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
A single somatic FOXL2 mutation (FOXL2(C134W)) was identified in almost all granulosa cell tumor (GCT) patients. In the pituitary, FOXL2 and Smad3 coordinately regulate activin stimulation of follistatin transcription. We explored whether a similar regulation occurs in the ovary, and whether FOXL2(C134W) has altered activity. We show that in primary granulosa cells, GDF-9 and activin increase Smad3-mediated follistatin transcription. In contrast to findings in the pituitary, FOXL2 negatively regulates GDF-9 and activin-stimulated follistatin transcription in the ovary. Knockdown of endogenous FOXL2 confirmed this inhibitory role. FOXL2(C134W) displayed enhanced inhibitory activity, completely ablating GDF-9 and activin-induced follistatin transcription. GDF-9 and activin activity was lost when either the smad binding element or the forkhead binding element were mutated, indicating that both sites are required for Smad3 actions. This study highlights that FOXL2 negatively regulates follistatin expression within the ovary, and that the pathogenesis of FOXL2(C134W) may involve an altered interaction with Smad3.
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