Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Genome wide analysis of AR-associated factors and histone modifications in castration-resistant prostate cancer

ABSTRACT: Genome wide analysis of AR-associated factors and histone modifications in castration-resistant prostate cancer

PROVIDER: PRJNA509229 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR8310130.fastq.gz	Fastqsanger.gz
	SRR8310131.fastq.gz	Fastqsanger.gz
	SRR8310132.fastq.gz	Fastqsanger.gz
	SRR8310133.fastq.gz	Fastqsanger.gz
	SRR8310134.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 10

Similar Datasets

Genome wide analysis of AR-associated factors and histone modifications in castration-resistant prostate cancer

Project description:Prostate cancer is the most common cancer in men and androgen receptor (AR) downstream signalings promote prostate cancer progression. Although androgen deprivation therapy is effective for treating prostate cancer, most of tumors relapsed as castration-resistant prostate cancer (CRPC). We performed ChIP-seq analysis to investigate the role of AR-associated factors and histone modifications using CRPC model cells, 22Rv1.

2019-04-01 | GSE123565 | GEO

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 signalling in castration resistant prostate cancer (CRPC)

Project description:Castration-resistant PCa (CRPC) remains androgen receptor (AR) dependent. There are multiple mechanisms for reactivation of AR including expression of the constitutively active AR splice variant, AR-V7 (AR3). Earlier studies suggest that though the variants regulate many of the same genes as AR, they also have unique targets. Another argument is that the variant is a “weak” AR without unique targets. We have used an LN95 cell line that endogenously expresses AR and a low level of AR-V7 to compare the activities of the isoforms and to determine whether there is differential regulation of target genes. The transcriptomes for AR and AR-V7 were identified using RNA-Seq.

2021-12-31 | GSE184676 | GEO

Bypass mechanisms of the AR pathway in castration-resistant PC346 prostate cancer cells

2010-10-21 | GSE21596 | GEO

Bypass mechanisms of the AR pathway in castration-resistant PC346 prostate cancer cells

Project description:Prostate cancer is initially dependent on androgens for survival and growth, making hormonal therapy the cornerstone treatment for invasive tumors. However, despite initial remission, the cancer will inevitably recur. The present study was set to investigate how androgen-dependent prostate cancer cells eventually survive and resume growth under androgen-deprived and antiandrogen supplemented conditions Microarray technology was used to analyze differences in gene expression between androgen-responsive and hormone-refractory prostate cancer cell lines. As model system, we used the androgen-responsive PC346C cells and its castration-resistant sublines: PC346DCC, PC346Flu1 and PC346Flu2. These sublines were derived from the parental PC346C by long-term androgen ablation (PC346DCC), supplemented with the antiandrogen hydroxyflutamide (PC346Flu1 and PC346Flu2). Previous studies revealed distinct AR modifications in all three castration-resistant sublines: AR overexpression (PC346Flu1), AR down-regulation (PC346DCC) and T877A AR mutation (PC346Flu2). Each of the hormone-refractory sublines were cultured in their respective selection medium (steroid-stripped medium for PC346DCC, supplemented with 1 mM OH-Flutamide for PC346Flu1 and Flu2) and hybridized on the microarrays, together with the parental androgen-responsive PC346C (cultured in complete medium supplemented with 0.1 nM R1881). To account for the biological variability and dye-preferential binding to oligonucleotides on the microarray, four replicate arrays were performed per cell line, using two independent cell passages in dye-swap.

2010-10-21 | E-GEOD-21596 | biostudies-arrayexpress

AR signalling in castration resistant prostate cancer (CRPC)

Project description:AR signalling in castration resistant prostate cancer (CRPC)

| PRJNA765614 | ENA

Transcriptome profiling of castration resistant prostate cancer cells treated with novel AR N-terminal inhibitor

Project description:This study aimed at exploring how would the novel AR N-terminal inhibitor affect the androgen receptor (AR) transcriptome, especially a subset of genes that are uniquely upregulated by AR-V7 in castration resistant prostate cancer cells. We performed next-generation sequencing-based gene expression profiling (RNA-sequencing) on the castration-resistant prostate cancer celll line LNCaP-95. LNCaP-95 expresses high level of endogeneous AR-V7, and also acquired an adaptive shift towards AR-V7-mediated AR signaling activity. Beside regulating the transcription of a subset of canonical wildtype AR genes, AR-V7 also mediates a distinct transcriptional program that is independent of wildtype AR in LNCaP-95. In this experiment, LNCaP-95 cells were treated with vehicle control or the AR-N terminal inhibitor SC912. The subsequent AR transcriptomic change following compound treatment, especially the AR-V7 unique genes were assessed by RNA-seq.

2024-04-30 | GSE253122 | GEO

Hes6 drives a critical AR transcriptional program to induce castration resistant prostate cancer through activation of an E2F1-mediated cell cycle network

Project description:Castrate-resistant prostate cancer (CRPC) is poorly characterized and heterogeneous and while the androgen receptor (AR) is of singular importance, other factors such as c-Myc and the E2F family also play a role in later stage disease. Here we show that Hes6 is up-regulated in aggressive human prostate cancer and drives castration-resistant tumour growth in the absence of ligand binding by enhancing the transcriptional activity of the AR, which is preferentially directed to a regulatory network enriched for other transcription factors including E2F1. In the clinical setting, we have uncovered a Hes6-associated signature that predicts poor outcome in prostate cancer, which can be pharmacologically targeted with restoration of sensitivity to castration. AR and E2F1 ChIPseq from multiple simultaneous LNCaP cell replicates with and without bicalutamide

2014-04-17 | E-GEOD-49832 | biostudies-arrayexpress

Transcriptome profiling of castration-resistant prostate cancer cells treated with novel androgen receptor (AR) and AR-V7 inhibitors

Project description:The purpose of this study was to characterize the downstream transcriptomic effects of ARVib-mediated degradation of AR/AR-V7, particularly in attenuating AR/AR-V7 target gene expression in prostate cancer cells. Towards this goal, next-generation sequencing (NGS)-based gene expression profiling (RNA-Sequencing; RNA-Seq) was performed on castration-resistant prostate cancer (CRPC) C4-2B MDVR cells that were treated with vehicle control or one of the AR/AR-V7 inhibitors (ARVib), ARVib-7 or ARVib-31.

2021-08-22 | GSE158556 | GEO

AR-V7 Targets in Castration-Resistant Prostate Cancer (CRPC) Cell Line

Project description:In order to define the genes responsible for the growth and survival of a human castration-resistant prostate cancer cell line, a short term (doxycycline inducible) knockdown system was developed and utilized. Three independent 22Rv1 cell isolates were derived for each of the following doxycycline-inducible shRNAs (shGFP, shAR3, and shVav3) (AR3 = AR-V7). The cells were grown in androgen depleted conditions, plus or minus doxycycline, for three days. RNA from the 18 samples was then sent to the University of Miami Genetics Core for RNA Integrity Number (RIN) evaluation and microarray analysis. Genes differentially regulated by AR-V7 knock-down or VAV3 knock-down were explored as downstream targets of AR-V7 or VAV3, respectively.

2018-08-16 | GSE104572 | 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