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Loss of CHD1 promotes chromatin dysregulation leading to heterogeneous mechanisms of resistance to hormone therapy in prostate cancer [shRNA screen]

ABSTRACT: Loss of CHD1 promotes chromatin dysregulation leading to heterogeneous mechanisms of resistance to hormone therapy in prostate cancer [shRNA screen]

PROVIDER: PRJNA525865 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8690630.fastq.gz	Fastqsanger.gz
	SRR8690640.fastq.gz	Fastqsanger.gz
	SRR8690650.fastq.gz	Fastqsanger.gz
	SRR8690660.fastq.gz	Fastqsanger.gz
	SRR8690670.fastq.gz	Fastqsanger.gz

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Loss of CHD1 promotes chromatin dysregulation leading to heterogeneous mechanisms of resistance to hormone therapy in prostate cancer [shRNA screen]

Project description:Next generation androgen receptor (AR) signaling inhibitors have significantly improved the survival of men with metastatic castration-resistant prostate cancer (mCPRC) but resistance remains a problem. Genomic alterations at the AR locus are present in ~50% of mCRPC patients, typically in association with large numbers of copy number gains and losses across the genome. To explore the functional consequences of these copy number alterations, we screened an shRNA library targeting all genes deleted in prostate cancer (the prostate cancer deletome: 4380 shRNAs targeting 730 genes) for next generation antiandrogen resistance using a clinically-validated model of enzalutamide-sensitive, AR-driven mCRPC LNCaP/AR. The Chromatin helicase DNA-binding factor (CHD1) scored as a top candidate and was validated in vitro and in vivo using multiple independent shRNAs and CRISPR guides. Mechanistically, CHD1 loss led to global changes in open and closed chromatin (ATAC-seq) as well as downregulation of canonical AR target genes upon the challenge of antiandrogen, despite robust AR expression. Integrative analysis of ATAC- and RNA-seq changes following CHD1 deletion identified 23 candidate transcription factor drivers of enzalutamide resistance. CRISPR-based unbiased functional screening identified 4 of these drivers may drive the AR-independent resistance, including glucocorticoid receptor (GR), BRN2, NR2F1 and TBX2. Genetic studies further establish that CHD1 loss confers antiandrogen resistance by converting mCRPC cells from AR-dependence to GR-dependence in one of the resistant LNCaP/AR clone. Thus, CHD1 functions as a molecular tuner to regulate chromatin plasticity and maintain oncogenic AR signaling, as well as AR dependency.

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Loss of CHD1 promotes chromatin dysregulation leading to heterogeneous mechanisms of resistance to hormone therapy in prostate cancer [ATAC-seq]

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Loss of CHD1 promotes chromatin dysregulation leading to heterogeneous mechanisms of resistance to hormone therapy in prostate cancer

Project description:Loss of CHD1 promotes chromatin dysregulation leading to heterogeneous mechanisms of resistance to hormone therapy in prostate cancer

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Loss of CHD1 promotes chromatin dysregulation leading to heterogeneous mechanisms of resistance to hormone therapy in prostate cancer [ATAC-seq]

Project description:Loss of CHD1 promotes chromatin dysregulation leading to heterogeneous mechanisms of resistance to hormone therapy in prostate cancer [ATAC-seq]

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Loss of CHD1 promotes chromatin dysregulation leading to heterogeneous mechanisms of resistance to hormone therapy in prostate cancer [RNA-seq]

Project description:Loss of CHD1 promotes chromatin dysregulation leading to heterogeneous mechanisms of resistance to hormone therapy in prostate cancer [RNA-seq]

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Expression data from Chd1-deficient mouse ES cells (E14 cell lines) and genome-wide binding of Chd1 in parental ES cells

Project description:We used microarrays to study the effect of Chd1 loss of function in mouse ES cells. We used ChIP-chip to analyze genome-wide binding of Chd1 in normal ES cells. Mouse Embryonic Stem (ES) cells were infected with a lentiviral vector (pSicoR-mCherry) for expression of a shRNA against Chd1 and GFP (as a control). mCherry-sorted ES cells were plated and individual clones were selected and grown under normal ES cell conditions. 6 ES cell clonal lines were isolated and analyzed along with the parental E14 cell line. The final analysis consisted in 3 control cell lines (E14, E1 and G8) and 4 Chd1-deficient cells (3 different clones using a shRNA sequence #1- C1i5, C1i6 and C1i9; 1 clone using a different shRNA (#4) sequence targeting Chd1- C4i2). RNA samples were isolated from these Chd1-deficient ES cells and control ES cells, and hybridized on Affymetrix chip. For ChIP-chip, parental E14 ES cell line was used.

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Loss of CHD1 promotes chromatin dysregulation leading to heterogeneous mechanisms of resistance to hormone therapy in prostate cancer

Project description:This SuperSeries is composed of the SubSeries listed below.

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Gene expression profiling of prostate cells with CHD1 knockdown

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