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Assembly of methylated LSD1 and CHD1 drives AR-dependent transcription and translocation

ABSTRACT: Assembly of methylated LSD1 and CHD1 drives AR-dependent transcription and translocation

OTHER RELATED OMICS DATASETS IN: PXD003262

PROVIDER: PRJNA271254 | ENA |

REPOSITORIES: ENA

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Dataset's files

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			Action	DRS
	SRR1735560_1.fastq.gz	Fastqsanger.gz
	SRR1735560_2.fastq.gz	Fastqsanger.gz
	SRR1735561_1.fastq.gz	Fastqsanger.gz
	SRR1735561_2.fastq.gz	Fastqsanger.gz
	SRR1735562_1.fastq.gz	Fastqsanger.gz

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Assembly of methylated LSD1 and CHD1 drives AR-dependent transcription and translocation [ChIP-Seq]

Project description:The aim of the study is to identify AR target gens in LNCaP cells 5 samples corresponding to LSD1 K114me2 or CHD1 genome-binding in DHT-treated and control LNCaP cells. 6 samples corresponding to LSD1 K114me2 or CHD1 genome-binding in LNCaP cells knocked-down for LSD1 or CHD1 and treated with DHT.

2015-12-07 | E-GEOD-64528 | biostudies-arrayexpress

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Project description:The aim of the study is to identify AR target gens in LNCaP cells 6 samples correponding to 2 times 3 replicates were used for the study

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Assembly of methylated LSD1 and CHD1 drives AR-dependent transcription and translocation [RNA-Seq]

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Assembly of methylated LSD1 and CHD1 drives AR-dependent transcription and translocation [ChIP-Seq]

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Loss of CHD1 facilitates oncogenic hijacking of AR during cancer progression [RNA-seq]

Project description:Deregulation of chromatin architecture is emerging as a critical feature of carcinogenesis, and genomic alterations in nucleosome remodelers are common in human cancer. Recurrent deletion of the chromatin remodeler CHD1 is among the most common alterations in prostate cancer, but its role as a tumor suppressor and the reasons for the tissue-specific nature of CHD1 deletion remain undefined. Here, we show that deletion of CHD1 drives prostate tumorigenesis and fundamentally reprograms the transcriptional program of the androgen receptor (AR), diverting AR towards an oncogenic transcriptional program and away from a growth suppressive transcriptome. Conditional deletion of Chd1 in mouse prostate resulted in prostate neoplasia in vivo, confirming CHD1 as a tumor suppressor in prostate tissue. In prostate cells, the interactome of chromatin-bound CHD1 was enriched for factors that regulate nuclear receptor function, and interrogation of the CHD1 cistrome revealed promoter-independent enrichment of CHD1 at sites specifically occupied by AR and its associated transcriptional regulators. Deletion of CHD1 resulted in a dramatic redistribution of AR across the genome, localizing AR to sites enriched for HOXB13, and depleting AR at AR-halfsite motifs, consistent with the AR cistrome and epigenetic marks in human prostate cancer samples. Furthermore, the CHD1 null AR cistrome was associated with a unique AR transcriptional signature, enriched for pro-oncogenic pathways and depleted for processe consistent with normal prostatic function. Collectively, these data implicate CHD1 as a prostate-specific tumor suppressor which constrains the oncogenic functions of AR though maintenance of a normal AR transcriptional program.

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Assembly of methylated LSD1 and CHD1 drives AR-dependent transcription and translocation

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2015-12-07 | E-GEOD-64530 | biostudies-arrayexpress

Assembly of methylated LSD1 and CHD1 drives AR-dependent transcription and translocation

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

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Project description:Assembly of methylated LSD1 and CHD1 drives AR-dependent transcription and translocation [RNA-Seq]

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Homo sapiens

Project description:Assembly of methylated LSD1 and CHD1 drives AR-dependent transcription and translocation [ChIP-Seq]