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BRD4 ChIP-Seq in 22Rv1 cells exogenously expressing HNF4G or GFP

ABSTRACT: BRD4 ChIP-Seq in 22Rv1 cells exogenously expressing HNF4G or GFP

PROVIDER: PRJNA1072116 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27840887_1.fastq.gz	Fastqsanger.gz
	SRR27840887_2.fastq.gz	Fastqsanger.gz
	SRR27840888_1.fastq.gz	Fastqsanger.gz
	SRR27840888_2.fastq.gz	Fastqsanger.gz
	SRR27840889_1.fastq.gz	Fastqsanger.gz

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BRD4 ChIP-Seq in 22Rv1 cells exogenously expressing HNF4G or GFP

Project description:BRD4 ChIP-Seq in 22Rv1 cells exogenously expressing HNF4G or GFP

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Expression profile of 22Rv1 cells with GFP or HNF4G exogenous expression when treated with BETi ABBV-075

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HNF4G, AR, FOXA1, H3K4me1, H3K27acetyl binding sites upon knockdown and overexpression of HNF4G in 22Rv1 and LNCaP prostate cancer cells respectively

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Project description:Despite recent advances in the treatment of pancreatic adenocarcinoma (PDAC), clinical outcome remains poor. Previous evidence linked the pioneer transcription factor FOXA1 as a mediator of new regulatory elements that drive tumour progression in models of late-stage disease. Given the critical role of FOXA1 as a pioneer factor for nuclear receptor (NR) transcription factors (TF) in breast and prostate cancer (Estrogen Receptor and Androgen Receptor), we hypothesised that FOXA1 might function with a NR in PDAC (1) (2). Using RIME, our unbiased approach for discovering endogenous protein complexes, we identified HNF4A and HNF4G as reproducible, FOXA1-associated proteins, a finding that was validated in clinical samples of PDAC. Using complex and diverse PDAC models, we show that gene transcription in the classical subtype of pancreatic cancer is regulated by FOXA1/GATA5/6 and HNF4G. We show that HNF4G drives primary disease, in part by recruiting the methyltransferase PRMT1 to regulatory regions. In primary tumour context, HNF4G is the dominant protein and the presence of HNF4G masks FOXA1 activity, resulting in FOXA1 being present, but functionally redundant in primary disease. During transition to metastasis however, HNF4G expression decreases, which unmasks FOXA1 activity, where it becomes transcriptionally active and a subsequent driver of metastasis. We provide new molecular insight into the key TFs in PDAC and the stage-specific activity of these proteins.

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Gene expression profile of LNCaP prostate cancer cells with exogenous HNF4G expression

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22Rv1 in vivo progression model

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