Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Investigation of the AR cistrome in response to RB depletion in castration-resistant prostate cancer

ABSTRACT: Investigation of the AR cistrome in response to RB depletion in castration-resistant prostate cancer

PROVIDER: PRJNA719828 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR14145981.fastq.gz	Fastqsanger.gz
	SRR14145982.fastq.gz	Fastqsanger.gz
	SRR14145983.fastq.gz	Fastqsanger.gz
	SRR14145984.fastq.gz	Fastqsanger.gz
	SRR14145985.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 6

Similar Datasets

Investigation of the AR cistrome in response to RB depletion in castration-resistant prostate cancer

Project description:These studies examine the consequence of RB loss on AR function in late stage disease

2022-04-01 | GSE171511 | GEO

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

Project description:The molecular drivers for the AR signaling reprogramming in castration-resistant prostate cancer remain to be determined. In this study, we hypothesize that increased AR expression in conjunction with lower-level androgens, which is a typical condition in prostate cancer cells receiving androgen deprivation therapy, is a major driving force of the reprogramming. To test this, we used LNCaP model with inducible overexpression of AR to examine the acute effects of AR overexpression stimulated by low-dose DHT (0.1nM) on AR cistrome.

2022-11-21 | GSE211639 | GEO

Cistrome analyses of AR-V7.

Project description:Cistrome analyses of AR-V7.

| PRJNA913106 | ENA

MECOM: A novel player in AR-driven Treatment Resistant Castration-Resistant Prostate Cancer

Project description:Reprogramming of the androgen receptor (AR) cistrome is associated with disease progression, and advanced castrate-resistant prostate cancers (CRPC) tend to rely on a reprogrammed/non-canonical AR signaling that is addictive to AR signaling inhibitor (ARSI) resistance. We identified EVI1, an oncogenic nuclear transcription factor, EVI1 coded by MECOM, as a novel AR-recruited co-activator for non-canonical signaling. In prostate cancer, MECOM is exclusively overexpressed in CRPC and enzalutamide-resistant CRPC and interacts with AR in the nucleus. MECOM knockdown cells exhibited decreased proliferation, aberration of critical cell survival transcriptional programs, suppressed super-enhancer (SE) activity, and increased pro-apoptotic signatures. Intriguingly, MECOM overexpression is vulnerable to PARP inhibitors regardless of DDR or HRR gene mutation status. These insights uncover the mechanistic role of MECOM in AR reprogrammed cistrome for cell survival and its vulnerability. More importantly, this study suggests that MECOM overexpression may be another biomarker that could significantly broaden the use of PARP inhibitors beyond those with HRR gene mutations.

2026-06-08 | PXD062331 | Pride

GNL3 orchestrates AR transcriptional programs to drive castration-resistant prostate cancer and immune evasion

Project description:Androgen receptor (AR) signaling is a primary oncogenic driver of castration-resistant prostate cancer (CRPC), yet the mechanism remains incompletely understood. Dysregulation of the AR co-regulatory network has emerged as a key driver of castration resistance. To identify AR-interacting proteins linked to CRPC progression, we performed proteomics-based rapid immunoprecipitation of endogenous proteins (RIME) analysis targeting AR in the CRPC cell line C4-2B.

2026-06-08 | PXD067138 | Pride

AR cistrome in satellite cells (NT)

Project description:Determine AR cistrome in satellite cells and correlate it with the presence of H3K27ac and H3K4me2

2026-08-21 | GSE303620 | GEO

AR cistrome in satellite cells (NT)

Project description:AR cistrome in satellite cells (NT)

| PRJNA1295934 | ENA

Spermine is a natural suppressor of AR signaling in castration-resistant prostate cancer

Project description:In castration-resistant prostate cancer (CRPC), clinical response to androgen receptor (AR) antagonists is limited mainly due to AR-variants expression and restored AR signaling. The metabolite spermine is most abundant in prostate and it decreases as prostate cancer progresses, but its functions remain poorly understood. Here, we show spermine inhibits full-length androgen receptor (AR-FL) and androgen receptor splice variant 7 (AR-V7) signaling and suppresses CRPC cell proliferation by directly binding and inhibiting protein arginine methyltransferase PRMT1. Spermine reduces H4R3me2a modification at the AR locus and suppresses AR binding as well as H3K27ac modification levels at AR target genes. Spermine supplementation restrains CRPC growth in vivo. PRMT1 inhibition also suppresses AR-FL and AR-V7 signaling and reduces CRPC growth. Collectively, we demonstrate spermine as an anticancer metabolite by inhibiting PRMT1 to transcriptionally inhibit AR-FL and AR-V7 signaling in CRPC, and we indicate spermine and PRMT1 inhibition as powerful strategies overcoming limitations of current AR-based therapies in CRPC.

2023-10-11 | MTBLS8034 | MetaboLights

AR cistrome in satellite cells [day 5]

Project description:Determine AR cistrome in satellite cells and correlate it with the presence of H3K27ac and H3K4me2

2026-08-21 | GSE303615 | GEO

Cistrome analyses of AR-V7.

Project description:Although AR-V7 has been intensively studied, it remains unclear whether AR-V7 can specifically activate a distinctive transcriptional program from the full-length AR (AR-FL), and whether AR-V7 may play a role in accelerating the metastatic progression of castration-resistant PCa (CRPC). In this study, we hypothesize that AR-V7 can drive a distinct transcription program from AR-FL in CRPC condition. To test this, we used LNCaP model with inducible overexpression of AR-V7 or AR-FL to examine the effects of AR-V7 overexpression or AR-FL overexpression stimulated with DHT for 4 hours on AR-V7 or AR-FL cistromes. We also studied the effects of AR-V7 on cistromes of pioneer factor FOXA1 and active histone marker H3K27ac, and the function of phosphorylation at Ser81 on AR-V7 function in CRPC.

2024-06-05 | GSE221140 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data