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

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

PROVIDER: PRJNA524393 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8639450_1.fastq.gz	Fastqsanger.gz
	SRR8639450_2.fastq.gz	Fastqsanger.gz
	SRR8639460_1.fastq.gz	Fastqsanger.gz
	SRR8639460_2.fastq.gz	Fastqsanger.gz
	SRR8639451_1.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

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 [shRNA screen]

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

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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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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.

2020-03-26 | GSE127957 | GEO

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

2020-03-26 | GSE127241 | GEO

Loss of CHD1 promotes chromatin dysregulation leading to heterogeneous mechanisms of resistance to hormone therapy in prostate cancer [RNA-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:This SuperSeries is composed of the SubSeries listed below.

2020-03-26 | GSE126918 | GEO

Gene expression profiling on heads of Drosophila chromodomain helicase DNA binding protein 1 (CHD1) deletion mutants

Project description:CHD1 is a conserved ATP-dependent chromatin remodeling factor with roles in transcriptional regulation and chromatin assembly. Here we show that deletion of Chd1 causes multiple behavioral and metabolic defects. In particular, it diminishes food-intake and results in shortened lifespan of mutant flies. These phenotypes can be rescued by brain-specific expression of Chd1 via the elav promoter. Consistently, neuron-specific expression of Chd1 rescues the wide-spread transcriptional dysregulation observed in the absence of CHD1.

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Microarray of CHD1 Knockdown in PC3 cells and CHD1 knockout in LNCaP cells

Project description:We used microarrays to study the global gene expression and identified differentially expressed genes in CHD1 knockdown PC-3 cells and CHD1 KO LNCaP cells, aiming to identify genes and pathways that are regulated by CHD1

2017-02-10 | GSE84970 | GEO

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