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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.

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

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

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

Project description:Hepatocellular carcinoma (HCC) is sexually dimorphic in both rodents and humans, with significantly higher incidence in males, an effect that is dependent on sex hormones. The molecular mechanisms by which estrogens prevent and androgens promote liver cancer remain unclear. Here, we discover that sexually dimorphic HCC is completely reversed in Foxa1- and Foxa2-deficient mice after diethylnitrosamine-induced hepatocarcinogenesis. Coregulation of target genes by Foxa1/a2 and either the estrogen receptor (ERα) or the androgen receptor (AR) was increased during hepatocarcinogenesis in normal female or male mice, respectively, but was lost in Foxa1/2-deficient mice. Thus, both estrogen-dependent resistance to and androgen-mediated facilitation of HCC depend on Foxa1/2. Strikingly, single nucleotide polymorphisms at FOXA2 binding sites reduce binding of both FOXA2 and ERα to their targets in human liver and correlate with HCC development in women. Thus, Foxa factors and their targets are central for the sexual dimorphism of HCC.

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