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Foxa1 and Foxa2 are essential for gender dimorphism in liver cancer

ABSTRACT: Foxa1 and Foxa2 are essential for gender dimorphism in liver cancer

PROVIDER: PRJEB2771 | ENA |

REPOSITORIES: ENA

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			Action	DRS
		Other
	ERR056354.fastq.gz	Fastqsanger.gz
	ERR056355.fastq.gz	Fastqsanger.gz
	ERR056356.fastq.gz	Fastqsanger.gz
	ERR056357.fastq.gz	Fastqsanger.gz

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Foxa1 and Foxa2 are essential for gender dimorphism in liver cancer

Project description:Foxa1loxP/loxP;Foxa2loxP/loxP and Foxa1loxP/loxP;Foxa2loxP/loxP;AfpCre mice of both genders were treated with or without carcinogen to induce liver cancer. ChIP-Seq was performed in the liver samples after cross-linking. ChIP-DNA was sequenced with the Illumina GAII sequencer. The AfpCre when present knocks out the Foxa1 and Foxa2 genes, so removing the corresponding proteins.

2012-02-24 | E-MTAB-805 | biostudies-arrayexpress

Targeting FOXA1 and FOXA2 Disrupts the Lineage-Specific Oncogenic Output in Prostate Cancer

Project description:Activation of the androgen receptor (AR) is the key lineage-specific oncogenic pathway and the primary therapeutic target in prostate cancer. While AR signaling is enabled by the pioneer transcription factor FOXA1, its homolog FOXA2 is specifically expressed in advanced lineage plasticity prostate cancers that have lost the AR signaling axis. However, their roles and utility as drug targets remain incompletely characterized. Here, we show an unexpected collaboration of FOXA1 and FOXA2 in mediating AR-independent cell proliferation in different lineage plasticity cancer subtypes. Conversely, joint loss-of-function or pharmacologic disruption of FOXA1 and FOXA2 leads to the collapse of lineage-specific oncogenic transcription factors followed by cell cycle arrest. In summary, our findings uncover a druggable dependency for AR-positive and -negative prostate cancers.

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Foxa1 and Foxa2 are Required for Sexual Dimorphism in Liver Cancer - Gene Expression

Project description:Gene expression changes between livers of treated WT and dKO (Foxa1 and Foxa2 KO) male and female mice and untreated female (WT and dKO) mice were measured to identify pathways related to Foxa1/2 regulation of pathways involved in liver cancer. The experiment uses 4 replicates each for 6 conditions

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Foxa1 and Foxa2 are essential for sexual dimorphism in liver cancer.

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Project description:FOXA1 and FOXA2 are essentail transcription factors for proper gut development. In adults, they have a role in the differentiation of intestinal secretory cell lineages and were also reporeted to directly activate Muc2 transcription. Here we show that deletion of Foxa1 and Foxa2 in mouse intestinal epithelium leads to a downregulation of glycosylation genes in the colon and to a massive change of the colonic surface glycans. In turn, the microbiome composition shifts dramatically and spontaneous inflammatory bowel disease ensued. We conclude that vertebrates shape a favorable microbiome by establishing a glycocalyx to nurture specific bacterial taxa through control of the epithelial glycosylation program by the FoxA transcription factors.

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Regulatory cistrome landscape of Foxa1 and Foxa2 during prostate cancer progression [ChIP-seq]

Project description:To characterize the genome-wide regulatory cistrome of Foxa1 and Foxa2, we performed both Foxa1 and Foxa2 chromatin immunoprecipitation followed by sequencing (ChIP-seq) on freshly dissociated prostate tumor cells at the early stage (2 weeks post tamoxifen administration) and the late stage (6 months post tamoxifen administration) of NEPC progression, respectively.

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FOXA1 and FOXA2 binding profile in mouse colon [ChIP]

Project description:FOXA1 and FOXA2 are essentail transcription factors for proper gut development. In adults, they play a role in the differentiation of intestinal secretory cells and were also reporeted to directly activate Muc2 transcription. Here we show that FOXA1 and FOXA2 bind near goblet cell genes, and are specifically enriched near glycosylation genes. Deletion of these transcription factors in mouse intestine leads to a downregulation of glycosylation genes in the colon and to a massive change of the colonic surface glycans. I turn, the microbiome composition shifts dramatically and spontaneous inflammatory bowel disease ensued. We conclude that vertebrates shape a favorable microbiome by establishing a glycocalyx to nurture specific bacterial taxa through control of the epithelial glycosylation program by the FoxA transcription factors.

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