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Global transcriptomic analysis of murine ovarian surface epithelial (MOSE) cells with PAX8 overexpression

ABSTRACT: Global transcriptomic analysis of murine ovarian surface epithelial (MOSE) cells with PAX8 overexpression

PROVIDER: PRJNA528763 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8774320.fastq.gz	Fastqsanger.gz
	SRR8774315.fastq.gz	Fastqsanger.gz
	SRR8774316.fastq.gz	Fastqsanger.gz
	SRR8774317.fastq.gz	Fastqsanger.gz
	SRR8774318.fastq.gz	Fastqsanger.gz

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Global transcriptomic analysis of murine ovarian surface epithelial (MOSE) cells with PAX8 overexpression

Project description:To identify the role of PAX8 in transformation of the ovarian surface epithelium (OSE).

2019-10-01 | GSE128751 | GEO

Epigenomic remodeling of the PAX8 cistrome in high grade serous ovarian cancer [ChIP-Seq]

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Epigenomic remodeling of the PAX8 cistrome in high grade serous ovarian cancer [RNA-Seq]

Project description:We report mapping of the PAX8 cistrome in three high grade serous ovarian cancer cell lines (KURAMOCHI, OVSAHO, and JHOS4) compared to three benign immortalized fallopian tube cell lines (FT33, FT194, and FT246). We identified a highly conserved PAX8 binding pattern common across benign fallopian tube cell lines that was distinct from the unique PAX8 binding patterns seen in each cancer cell line. Comparison of benign and malignant Mullerian cell lines with and without PAX8 knockdown. For each cell line, three distinct siRNAs targeting PAX8 plus a pool of all three siRNAs were examined and compared to both a non-transfected control as well as a control transfected with a non-targeting siRNA.

2016-08-08 | E-GEOD-83100 | biostudies-arrayexpress

PAX8 interacts with the SWI/SNF complex at enhancers to drive proliferation in ovarian cancer

Project description:Activation of lineage-specific gene expression programs is mediated by the sequence-specific recruitment of transcriptional coactivators to chromatin. This occurs via interaction with lineage specific DNA binding transcription factors. The lineage factor PAX8 drives essential gene expression in ovarian cancer cells and is required for tumor proliferation. However, the molecular details surrounding co-factor recruitment and specific activation of transcription by PAX8 remain unknow. Here, we identify an important functional interaction between PAX8 and the Switch/Sucrose Non-Fermentable (SWI/SNF) chromatin remodeling complex. We show that PAX8 can recruit SWI/SNF complexes to DNA, where they function to open chromatin and facilitate expression of PAX8 target genes. Genetic deletion of PAX8 results in loss of SWI/SNF from PAX8 bound enhancers, loss of expression of associated target genes, and reduced proliferation. These results can be phenocopied by pharmacological inhibition of SWI/SNF ATPase activity. These data indicate that PAX8 mediates the expression of an essential ovarian cancer proliferative program in part by the recruitment of chromatin remodelers.

2024-08-04 | GSE272992 | GEO

Epigenomic remodeling of the PAX8 cistrome in high grade serous ovarian cancer [RNA-Seq]

2016-08-08 | GSE83100 | GEO

Epigenomic remodeling of the PAX8 cistrome in high grade serous ovarian cancer [ChIP-Seq]

2016-08-08 | GSE79893 | GEO

PAX8 interacts with the SWI/SNF complex at enhancers to drive proliferation in ovarian cancer [ChIP-seq]

2024-08-04 | GSE273024 | GEO

Transcriptional profile of stemness in the ovarian surface epithelium

Project description:We leverage RNA sequencing to identify the transcriptional changes assocaited with several experimental conditions that induce a stemness phenotype in the ovarian surface epithelium, including spheroid culture, Snail overexpression, and BRCA1 deletion

2020-06-01 | GSE122875 | GEO

Candidate genes and pathways downstream of PAX8 involved in ovarian high-grade serous carcinoma

Project description:Our goal was to identify candidate genes and pathways regulated by PAX8 that could be additional targets for the therapy of ovarian carcinoma. To reach this aim, we have determined the molecular profiles of ovarian cancer cells and in parallel of Fallopian tube epithelial cells by mean of a silencing approach followed by an RNA-seq analysis

2016-09-23 | GSE79572 | GEO

Both Fallopian Tube and Ovarian Surface Epithelium Can Act as Cell-of-Origin for High Grade Serous Ovarian Carcinoma

Project description:The cell-of-origin of high grade serous ovarian carcinoma (HGSOC) remains controversial, with fallopian tube epithelium (FTE) and ovarian surface epithelium (OSE) both considered candidates. Here, by using genetically engineered mouse models and organoids, we assessed the tumor-forming properties of FTE and OSE harboring the same oncogenic abnormalities. Combined RB family inactivation and Tp53 mutation in Pax8+ FTE caused Serous Tubal Intraepithelial Carcinoma (STIC), which metastasized rapidly to the ovarian surface. These events were recapitulated by orthotopic injection of mutant FTE organoids. Engineering the same genetic lesions into Lgr5+ OSE or OSE-derived organoids also caused metastatic HGSOC, although with longer latency and lower penetrance. FTE- and OSE-derived tumors had distinct transcriptomes, and comparative transcriptomics and genomics suggest that human HGSOC arises from both cell types. Finally, FTE- and OSE-derived organoids exhibited differential chemosensitivity. Our results comport with a dualistic origin for HGSOC and suggest that the cell-of-origin might influence therapeutic response.

2019-10-21 | GSE125016 | GEO

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