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FOXO1 mitigates the SMAD3/FOXL2C134W transcriptomic effect in a model of human adult granulosa cell tumor

ABSTRACT: Granulosa cell tumors (GCTs) are a rare form of stromal cell malignant cancer accounting for one in twenty cases of ovarian cancer. More than 400 tumors from aGCT patients of diverse ethnicities showed one single mutation in the Forkhead box L2 transcription factor gene FOXL2: Cys134Trp (c.402C

ORGANISM(S): Homo sapiens

PROVIDER: GSE166794 | GEO | 2021/02/26

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.

2012-11-05 | GSE39890 | GEO

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

2012-11-05 | E-GEOD-39890 | biostudies-arrayexpress

FOXO1 mitigates the SMAD3/FOXL2C134W transcriptomic effect in a model of human adult granulosa cell tumor

Project description:FOXO1 mitigates the SMAD3/FOXL2C134W transcriptomic effect in a model of human adult granulosa cell tumor

| PRJNA701969 | ENA

The oncogenic FOXL2 mutation C134W is the sole driver of granulosa cell tumors in mice

Project description:We have generated a humanized Foxl2 mouse model by genome editing to evaluate in vivo the role of mutated FOXL2 in the development of murine Adult Granulosa Cell Tumors

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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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FOXL2 and ESR1 binding sites in primary cells from mouse ovarian follicles

Project description:It has previously been shown that FOXL2 and ESR1 cooperate to repress the testis-determining gene Sox9 in murine granulosa cells, and suggested that FOXL2/ESR1 cooperation may be central to granulosa cell differentiation (Uhlenhaut et al., 2009). However, no study has so far compared the DNA-binding of FOXL2 and ESR1 at the genomic level or analyzed the impact of FOXL2 on ESR1 binding to its regulatory elements. Here, we have analyzed and compared the genomic locations recognized by ESR1 and FOXL2 in E2-treated primary murine granulosa cells. Input DNA, FOXL2 and ESR1 ChIP

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FOXL2 and ESR1 binding sites in primary cells from mouse ovarian follicles

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Comparative Genomic Hybridisation of 10 Ovarian Granulosa Cell tumors to ethnically-matched reference

Project description:We have performed a comparative genomic hybridization of 10 adult-type Ovarian Granulosa Cell tumors (GCTs) to obtain a picture of the genomic landscape of this cancer type and to identify new candidate driver genes. The samples are the somatic genomic DNA of 10 ovarian GCTs obtained from finnish patients. The reference DNA is an equimolar mix of genomic DNA from 10 finnish (ethnically-matched to sample DNAs) non-affected Females.

2015-11-30 | E-MTAB-2873 | biostudies-arrayexpress

A genome-wide exploration of the targets of the transcription factors FOXL2 and ESR2 unveils their implication in cell migration, invasion and adhesion [ChIP-Seq]

Project description:To explore what FOXL2-dependent changes of gene expression observed in our RNA-seq data were directly related to FOXL2 binding, we performed ChIP-seq analysis in FOXL2-expressing granulosa cells (two data points). To explore the potential co-regulation between FOXL2 and ESR2 of several targets, we knocked-down Esr2 in granulosa cells and performed a ChIP-seq under the same conditions as those previously described for FOXL2.

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Project description:Granulosa cell tumours (GCTs) of the ovary are a unique subset of ovarian stromal tumours accounting for approximately five percent of all ovarian malignancies. Based on their pathologic characteristics and clinical features, GCTs can be further divided into two distinct subtypes: adult-GCTs and juvenile-GCTs. In this study, we investigate the use of microRNAs (miRNAs) as potential biomarkers for the diagnosis and prognostication of GCTs.

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