ArticleBritish journal of cancer2024
A cellular model provides insights into the pathogenicity of the oncogenic FOXL2 somatic variant p.Cys134Trp.
Article in British journal of cancer, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 6 citations in OpenAlex.
- Modification of the Transcription Factor FOXL2 at Serines 101 and 107 Disables DNA Binding, Leads to Nucleolar Relocalization, and Rewires Granulosa-Cell Programs.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Assessing variant effect predictors and disease mechanisms in intrinsically disordered proteins.PLoS computational biology · 2025Article
- Regulation of FOXL2 gene in ovarian granulosa cell tumor by JNK inhibitor.Scientific reports · 2025Article
- CRISPR targeting of FOXL2 c.402C>G mutation reduces malignant phenotype in granulosa tumor cells and identifies anti-tumoral compounds.Molecular oncology · 2025Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
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Abstract
backgroundFOXL2 is a transcription factor expressed in ovarian granulosa cells. A somatic variant of FOXL2 (c.402 C > G, p.Cys134Trp) is the hallmark of adult-type granulosa cell tumours.
methodsWe generated KGN cell clones either heterozygous for this variant (MUT) or homozygous for the wild-type (WT) allele by CRISPR/Cas9 editing. They underwent RNA-Seq and bioinformatics analyses to uncover pathways impacted by deregulated genes. Cell morphology and migration were studied.
resultsThe differentially expressed genes (DEGs) between WT/MUT and WT/WT KGN cells (DEGs-
conclusionsOur work, aiming at better understanding the GOF scenario, shows that the dysregulated genes and pathways are consistent with this idea. Besides, we propose that GOF might result from an enhanced interaction with SMAD3 that could underlie an ectopic capacity of mutated FOXL2 to bind SMAD4.
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