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Response to supraphysiological testosterone is predicted by a distinct AR cistrome [RNA-seq]

ABSTRACT: Response to supraphysiological testosterone is predicted by a distinct AR cistrome [RNA-seq]

PROVIDER: PRJNA777878 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16771538_1.fastq.gz	Fastqsanger.gz
	SRR16771538_2.fastq.gz	Fastqsanger.gz
	SRR16771539_1.fastq.gz	Fastqsanger.gz
	SRR16771539_2.fastq.gz	Fastqsanger.gz
	SRR16771540_1.fastq.gz	Fastqsanger.gz

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Response to supraphysiological testosterone is predicted by a distinct AR cistrome

Project description:Response to supraphysiological testosterone is predicted by a distinct AR cistrome

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Response to supraphysiological testosterone is predicted by a distinct AR cistrome [ChIP-seq]

Project description:Response to supraphysiological testosterone is predicted by a distinct AR cistrome [ChIP-seq]

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Response to supraphysiological testosterone is predicted by a distinct AR cistrome

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

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Response to supraphysiological testosterone is predicted by a distinct AR cistrome [ChIP-seq]

Project description:We generated transcription factor, histone modification ChIP-Seq in CRPC PDX with SPT treatment

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Response to supraphysiological testosterone is predicted by a distinct AR cistrome [RNA-seq]

Project description:We generated RNA-Seq in CRPC PDX with SPT treatment

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Response to supraphysiological testosterone is predicted by a distinct androgen receptor cistrome.

Project description:The androgen receptor (AR) is a master transcription factor that regulates prostate cancer (PC) development and progression. Inhibition of AR signaling by androgen deprivation is the first-line therapy with initial efficacy for advanced and recurrent PC. Paradoxically, supraphysiological levels of testosterone (SPT) also inhibit PC progression. However, as with any therapy, not all patients show a therapeutic benefit, and responses differ widely in magnitude and duration. In this study, we evaluated whether differences in the AR cistrome before treatment can distinguish between SPT-responding (R) and -nonresponding (NR) tumors. We provide the first preclinical evidence to our knowledge that SPT-R tumors exhibit a distinct AR cistrome when compared with SPT-NR tumors, indicating a differential biological role of the AR. We applied an integrated analysis of ChIP-Seq and RNA-Seq to the pretreatment tumors and identified an SPT-R signature that distinguishes R and NR tumors. Because transcriptomes of SPT-treated clinical specimens are not available, we interrogated available castration-resistant PC (CRPC) transcriptomes and showed that the SPT-R signature is associated with improved survival and has the potential to identify patients who would respond to SPT. These findings provide an opportunity to identify the subset of patients with CRPC who would benefit from SPT therapy.

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Cistrome analyses of AR-V7.

Project description:Cistrome analyses of AR-V7.

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The impact of WDR77 on the AR cistrome in prostate cancer cells

Project description:Androgen receptor (AR) drives prostate cancer (CaP) even after androgen deprivation therapy (ADT) failed. Inhibiting AR’s transcription factor function to overcome acquired resistance to ADT is an attractive therapeutic avenue. However, which AR-coregulator interaction should be targeted is not clear, AR-coregulator complex higher order structures and stoichiometry are unknown, and how manipulating AR-coregulator interactions impacts the AR cistrome is not understood. Here, we examine interactions between AR and WD repeat 77 (WDR77, non-catalytic component of the methylosome complex), which are enriched in ADT-resistant CaP and mediate CaP cell survival. We performed CUT&RUN assays defined AR and WDR77 cistromes, the WDR77-dependence of the AR cistrome and the overlap between the AR and WDR77 cistromes in CaP cells.

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Cistrome analyses of AR stimulated by 0.1 nM DHT in LNCaP stable cell line overexpressing AR [ChIP-Seq]

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2022-11-21 | GSE211639 | GEO

Characterization of the AR cistrome in ER-negative breast cancer cell lines

Project description:Although molecular apocrine and some triple negative breast cancer tumours express high levels of AR, how AR signalling impacts their proliferative rate remains an area of controversy. The precise molecular mechanisms by which the AR can induce divergent proliferative effects in estrogen receptor-negative breast cancers has not been described. The potent androgen, DHT, inhibits proliferation of the MFM-223 estrogen receptor-negative breast cancer cell line. In contrast, activation of the AR by DHT either stimulates, or has no effect, on MDA-MB-453 cell proliferation. The AR cistrome was examined in order to identify candidate factors which mediate oncogenic versus tumour suppressive AR activity in ER-negative breast cancer.

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