ArticleMolecular and cellular endocrinology2013
Essential but differential role of FOXL2wt and FOXL2C134W in GDF-9 stimulation of follistatin transcription in co-operation with Smad3 in the human granulosa cell line COV434.
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 14 papers.
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Who cites it
14 citing papers in PubMed, 27 citations in OpenAlex.
- A cellular model provides insights into the pathogenicity of the oncogenic FOXL2 somatic variant p.Cys134Trp.British journal of cancer · 2024Article
- FOXO1 mitigates the SMAD3/FOXL2Journal of translational medicine · 2021Article
- New insights into testicular granulosa cell tumors.Oncology letters · 2020Review
- Article
- FOXO1 Negates the Cooperative Action of FOXL2Journal of the Endocrine Society · 2019Article
- New STAT3-FOXL2 pathway and its function in cancer cells.BMC molecular and cell biology · 2019Article
- Novel Polymorphisms inGenes · 2019Article
- Review
- Endogenous c-Jun N-terminal kinase (JNK) activity marks the boundary between normal and malignant granulosa cells.Cell death & disease · 2018Article
- FOXL2C134W-Induced CYP19 Expression via Cooperation With SMAD3 in HGrC1 Cells.Endocrinology · 2018Article
- Disruption of postnatal folliculogenesis and development of ovarian tumor in a mouse model with aberrant transforming growth factor beta signaling.Reproductive biology and endocrinology : RB&E · 2017Article
- SMAD3 Activation: A Converging Point of Dysregulated TGF-Beta Superfamily Signaling and Genetic Aberrations in Granulosa Cell Tumor Development?Biology of reproduction · 2016Review
- Article
- FOXL2, GATA4, and SMAD3 co-operatively modulate gene expression, cell viability and apoptosis in ovarian granulosa cell tumor cells.PloS one · 2014Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The FOXL2(C134W) mutation has been identified in virtually all adult granulosa cell tumors (GCTs). Here we show that the exogenous FOXL2 expression is necessary for GDF-9 stimulation of follistatin transcription in the human GCT cell line, COV434 that lacks endogenous FOXL2 expression. Interestingly, in the presence of Smad3 co-expression, FOXL2(C134W) negated GDF-9 stimulation of follistatin transcription. However, mutation of the Smad binding element (SBE) located in the intronic enhancer elements in the follistatin gene restored normal FOXL2 activity to FOXL2(C134W), thus the altered activity of FOXL2(C134W) is dependent on the ability of Smad3 to directly bind the SBE. Mutation of the FOXL2 binding element (FBE) or the FBE and SBE completely prevented GDF-9 activity, suggesting that the FBE is essential for GDF-9 stimulation in COV434. Overall, our study supports the view that altered interaction of FOXL2(C134W) with co-factors may underlie the pathogenesis of this mutation in GCTs.
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