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Effect of depletion of FOXL2 on gene expression in KGN cells

ABSTRACT: To investigate the targets of FOXL2 in human granulosa cells, we performed Knock-Down experiment in established homozygous cell lines for FOXL2 WT (KGN).

ORGANISM(S): Homo sapiens

PROVIDER: GSE227040 | GEO | 2023/11/06

REPOSITORIES: GEO

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Gene knockdown and overexpression of 402C>G FOXL2 in COV434 and KGN cells

Project description:Despite 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. The 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. 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. 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. Mutant FOXL2 was silenced in KGN cells with the use of siRNA and a non-targetting siRNA control. Wildtype and mutant FOXL2 were overexpressed in COV434 cells with the use of overexpression plasmids and an empty plasmid control. Each experiment was performed in triplicate. Total RNA was harvested at 24h post transfection and hybridised to Affymetrix U133 plus 2.0 arrays.

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ChIP-chip by array of human adult ovarian granulosa cell tumor derived cell line KGN using anti-FOXL2 antibodies

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Gene knockdown and overexpression of 402C>G FOXL2 in COV434 and KGN cells

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Transcription profiling of FOXL2 over-expression in human KGN cells

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Effect of depletion of FOXL2 on gene expression in KGN cells

Project description:Effect of depletion of FOXL2 on gene expression in KGN cells

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A cellular model of the oncogenic FOXL2 somatic pathogenic variant C134W provides new insights in pathogenicity

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FOXL2 interaction with different binding partners regulates the dynamics of granulosa cell differentiation across ovarian development

Project description:FOXL2 is a transcription factor essential for female fertility, expressed in somatic cells of the ovary, notably granulosa cells. In the mouse, Foxl2 deletion leads to partial sex reversal postnatally. However, deletion of the gene in 8-week-old females leads to granulosa to Sertoli cell transdifferentiation. We hypothesised that different outcomes of Foxl2 deletion in embryonic versus adult ovary may depend on a different role played across ovarian development. Therefore, we characterised the dynamics of gene expression and chromatin accessibility changes in purified murine granulosa cells across key developmental stages (E14.5, 1 and 8 weeks). We then performed genome-wide identification of FOXL2 target genes and on-chromatin interacting partners by ChIP-SICAP. We found that FOXL2 regulates more genes at postnatal stages, through the interaction with factors regulating primordial follicle activation (PFA), such as NR5A2, and others regulating steroidogenesis including AR and ESR2. As a proof of principle experiment, we chose one FOXL2 interactor, Ubiquitin specific protease 7 (USP7) and showed that deletion of this gene in granulosa cells leads to a blockage of PFA, impaired ovary development and sterility. Our study constitutes a comprehensive resource for exploration of the molecular mechanisms of ovarian development and causes of female infertility.

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