Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

SMAD3 promotes the expression and activity of androgen receptor in prostate cancer.

ABSTRACT: SMAD3 promotes the expression and activity of androgen receptor in prostate cancer.

PROVIDER: PRJNA873033 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR21229060_1.fastq.gz	Fastqsanger.gz
	SRR21229060_2.fastq.gz	Fastqsanger.gz
	SRR21229061_1.fastq.gz	Fastqsanger.gz
	SRR21229061_2.fastq.gz	Fastqsanger.gz
	SRR21229062_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 38

Similar Datasets

SMAD3 promotes the expression and activity of androgen receptor in prostate cancer [RNA-seq]

Project description:Overexpression of androgen receptor (AR) is the primary cause of castration-resistant prostate cancer, although mechanisms upregulating AR transcription in this context are not well understood. Our RNAseq studies revealed that SMAD3 knockdown decreased levels of AR and AR target genes, whereas SMAD4 or SMAD2 knockdown had little or no effect. ChIP-seq analysis showed that SMAD3 knockdown decreased global binding of AR to chromatin. Mechanistically, we show that SMAD3 binds to intron 3 of the AR gene to promote AR expression. Targeting these binding sites by CRISPRi reduced transcript levels of AR and AR targets. In addition, ~50% of AR and SMAD3 ChIP-seq peaks overlapped, and SMAD3 may also cooperate with or co-activate AR for AR target expression. Functionally, AR re-expression in SMAD3-knockdown cells partially rescued AR target expression and cell growth defects. The SMAD3 peak in AR intron 3 overlapped with H3K27ac ChIP-seq and ATAC-seq peaks in datasets of prostate cancer. AR and SMAD3 mRNAs were upregulated in datasets of metastatic prostate cancer and CRPC compared with primary prostate cancer. A SMAD3 PROTAC inhibitor reduced levels of AR, AR-V7 and AR targets in prostate cancer cells. This study suggests that SMAD3 could be targeted to inhibit AR in prostate cancer.

2023-01-12 | GSE211945 | GEO

SMAD3 promotes the expression and activity of androgen receptor in prostate cancer [CUT&RUN]

2023-01-12 | GSE211944 | GEO

SMAD3 promotes the expression and activity of androgen receptor in prostate cancer [RNA-seq]

Project description:SMAD3 promotes the expression and activity of androgen receptor in prostate cancer [RNA-seq]

| PRJNA873038 | ENA

SMAD3 promotes the expression and activity of androgen receptor in prostate cancer [CUT&RUN]

Project description:SMAD3 promotes the expression and activity of androgen receptor in prostate cancer [CUT&RUN]

| PRJNA873036 | ENA

Prostate cancer androgen receptor activity dictates efficacy of bipolar androgen therapy through MYC

Project description:Prostate cancer androgen receptor activity dictates efficacy of bipolar androgen therapy through MYC

| PRJNA880855 | ENA

Androgen receptor RIME in prostate cancer cells

Project description:Androgen receptor (AR) is a master transcription factor that drives prostate cancer (PCa) development and progression. Alterations in the expression or activity of AR coregulators significantly impact the disease's outcome. To identify all the essential components of the AR coregulator complex, we utilized a proteomic approach called rapid immunoprecipitation of endogenous proteins (RIME) to systematically identify all coregulator proteins of the AR interactome in PCa cells.

2022-07-12 | PXD031273 | Pride

Prostate Cancer Risk SNPs in Androgen Receptor Target Sites

Project description:We profiled androgen receptor (AR) genomic targets using high-throughput sequencing of chromatin-immunoprecipitated (ChIP) DNA from TMPRSS2-ERG fusion gene positive DUCaP prostate cancer cells. ChIp-seq and microarray gene expression profiling datasets were integrated with the NHGRI GWAS PCa risk SNPs catalog to identify disease susceptibility SNPs localized within functional androgen receptor binding sites (ARBSs). Eighty GWAS index or linked SNPs were found to be localized in ARBSs. Among these rs11891426:T>G in the 7th intron of the melanophilin gene was found located within a novel putative auxiliary AR binding motif, which we found enriched in the neighborhood of canonical androgen responsive elements. T→G exchange attenuated the transcriptional activity of the ARBS in an AR reporter gene assay of prostate cancer cell models. It went also in line with decreased melanophilin protein level in primary prostate tumors with G allele.These results unravel a hidden link between androgen receptor and a functional PCa risk SNP, whose allele alteration affects androgen regulation of its host gene melanophilin . Genomic profile of androgen receptor binding sites of androgen or vehicle treated DUCaP cells using ChIP-seq. IgG precipiated DNAs from both treatments served as controls.

2015-07-10 | E-GEOD-70679 | biostudies-arrayexpress

Neuropilin-2 regulates androgen-receptor transcriptional activity in advanced prostate cancer

Project description:Neuropilin-2 regulates androgen-receptor transcriptional activity in advanced prostate cancer

| PRJNA844001 | ENA

Prostate cancer androgen receptor activity dictates efficacy of bipolar androgen therapy through MYC [RNA-seq]

Project description:Testosterone is the canonical growth factor of prostate cancer but can paradoxically suppress its growth when present at supraphysiological levels. We have previously demonstrated that the cyclical administration of supraphysiological androgen (SPA), entitled Bipolar Androgen Therapy (BAT), can result in tumor regression and clinical benefit for patients with castration-resistant prostate cancer. However, predictors and mechanisms of response and resistance have been ill-defined. Here we show that growth inhibition of prostate cancer models by SPA requires high androgen receptor (AR) activity and is driven in part by downregulation of MYC. Using matched sequential patient biopsies, we show that high pre-treatment AR activity predicts downregulation of MYC, clinical response, and prolonged progression-free and overall survival for patients on BAT. BAT induced strong downregulation of AR in all patients, which is shown to be a primary mechanism of acquired resistance to SPA. Acquired resistance can be overcome by alternating SPA with the AR inhibitor enzalutamide, which induces adaptive upregulation of AR and re-sensitizes prostate cancer to SPA. This work identifies high AR activity score as a predictive biomarker of response to BAT and supports a new treatment paradigm for prostate cancer involving alternating between AR inhibition and activation

2022-11-01 | GSE213443 | GEO

Prostate cancer androgen receptor activity dictates efficacy of bipolar androgen therapy through MYC [ATAC-seq]

2022-11-01 | GSE213437 | GEO