ArticlePloS one2012
The transcriptional targets of mutant FOXL2 in granulosa cell tumours.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 75 citations in OpenAlex.
- Granulosa cell tumors and menopausal hormone therapy: A narrative review.Gynecologic oncology reports · 2026Review
- CRISPR targeting of FOXL2 c.402C>G mutation reduces malignant phenotype in granulosa tumor cells and identifies anti-tumoral compounds.Molecular oncology · 2025Article
- Gain-of-Function Chromatin Remodeling Activity of Oncogenic FOXL2C134W Reprograms Glucocorticoid Receptor Occupancy to Drive Granulosa Cell Tumors.Cancer research · 2025Article
- A cellular model provides insights into the pathogenicity of the oncogenic FOXL2 somatic variant p.Cys134Trp.British journal of cancer · 2024Article
- Article
- ERβ in Granulosa Cell Tumors and Its Clinical Potential.Endocrinology · 2023Review
- Forkhead box L2 is a target of miR-133b and plays an important role in the pathogenesis of non-small cell lung cancer.Cancer medicine · 2023Article
- Transcriptome profiling of banana shrimp (Fenneropenaeus merguiensis) ovaries and testes: Insights into FoxL2.PloS one · 2023Article
- Single-cell transcriptomic profiling provides insights into the toxic effects of Zearalenone exposure on primordial follicle assembly.Theranostics · 2021Article
- Single-cell transcriptome landscape of ovarian cells during primordial follicle assembly in mice.PLoS biology · 2020Article
- Genomic profiling of primary and recurrent adult granulosa cell tumors of the ovary.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2020Article
- Article
- The transcriptional regulator CBX2 and ovarian function: A whole genome and whole transcriptome approach.Scientific reports · 2019Article
- New STAT3-FOXL2 pathway and its function in cancer cells.BMC molecular and cell biology · 2019Article
- A novel mouse model of testicular granulosa cell tumors.Molecular human reproduction · 2018Article
- FOXL2C134W-Induced CYP19 Expression via Cooperation With SMAD3 in HGrC1 Cells.Endocrinology · 2018Article
- The molecular mechanism of ovarian granulosa cell tumors.Journal of ovarian research · 2018Review
- 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
- The disparate origins of ovarian cancers: pathogenesis and prevention strategies.Nature reviews. Cancer · 2017Review
- SMAD3 Activation: A Converging Point of Dysregulated TGF-Beta Superfamily Signaling and Genetic Aberrations in Granulosa Cell Tumor Development?Biology of reproduction · 2016Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundDespite their distinct biology, granulosa cell tumours (GCTs) are treated the same as other ovarian tumours. Intriguingly, a recurring somatic mutation in the transcription factor Forkhead Box L2 (FOXL2) 402C>G has been found in nearly all GCTs examined. This investigation aims to identify the pathogenicity of mutant FOXL2 by studying its altered transcriptional targets.
methodsThe expression of mutant FOXL2 was reduced in the GCT cell line KGN, and wildtype and mutant FOXL2 were overexpressed in the GCT cell line COV434. Total RNA was hybridised to Affymetrix U133 Plus 2 microarrays. Comparisons were made between the transcriptomes of control cells and cells altered by FOXL2 knockdown and overexpression, to detect potential transcriptional targets of mutant FOXL2.
resultsThe overexpression of wildtype and mutant FOXL2 in COV434, and the silencing of mutant FOXL2 expression in KGN, has shown that mutant FOXL2 is able to differentially regulate the expression of many genes, including two well known FOXL2 targets, StAR and CYP19A. We have shown that many of the genes regulated by mutant FOXL2 are clustered into functional annotations of cell death, proliferation, and tumourigenesis. Furthermore, TGF-β signalling was found to be enriched when using the gene annotation tools GATHER and GeneSetDB. This enrichment was still significant after performing a robust permutation analysis.
conclusionGiven that many of the transcriptional targets of mutant FOXL2 are known TGF-β signalling genes, we suggest that deregulation of this key antiproliferative pathway is one way mutant FOXL2 contributes to the pathogenesis of adult-type GCTs. We believe this pathway should be a target for future therapeutic interventions, if outcomes for women with GCTs are to improve.
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