Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

BRD9 is a critical regulator of androgen receptor signaling and prostate cancer progression - RNA-Seq

ABSTRACT: BRD9 is a critical regulator of androgen receptor signaling and prostate cancer progression - RNA-Seq

PROVIDER: PRJNA611535 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR11268469_1.fastq.gz	Fastqsanger.gz
	SRR11268469_2.fastq.gz	Fastqsanger.gz
	SRR11268470_1.fastq.gz	Fastqsanger.gz
	SRR11268470_2.fastq.gz	Fastqsanger.gz
	SRR11268471_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 96

Similar Datasets

BRD9 is a regulator of androgen receptor signaling and prostate cancer progression

Project description:BRD9 is a regulator of androgen receptor signaling and prostate cancer progression

| PRJNA611525 | ENA

BRD9 Is a Critical Regulator of Androgen Receptor Signaling and Prostate Cancer Progression.

Project description:Switch/sucrose-nonfermentable (SWI/SNF) chromatin-remodeling complexes are critical regulators of chromatin dynamics during transcription, DNA replication, and DNA repair. A recently identified SWI/SNF subcomplex termed GLTSCR1/1L-BAF (GBAF; or "noncanonical BAF", ncBAF) uniquely contains bromodomain-containing protein BRD9 and glioma tumor suppressor candidate region 1 (GLTSCR1) or its paralog GLTSCR1-like (GLTSCR1L). Recent studies have identified a unique dependency on GBAF (ncBAF) complexes in synovial sarcoma and malignant rhabdoid tumors, both of which possess aberrations in canonical BAF (cBAF) and Polybromo-BAF (PBAF) complexes. Dependencies on GBAF in malignancies without SWI/SNF aberrations, however, are less defined. Here, we show that GBAF, particularly its BRD9 subunit, is required for the viability of prostate cancer cell lines in vitro and for optimal xenograft tumor growth in vivo. BRD9 interacts with androgen receptor (AR) and CCCTC-binding factor (CTCF), and modulates AR-dependent gene expression. The GBAF complex exhibits overlapping genome localization and transcriptional targets as bromodomain and extraterminal domain-containing (BET) proteins, which are established AR coregulators. Our results demonstrate that GBAF is critical for coordinating SWI/SNF-BET cooperation and uncover a new druggable target for AR-positive prostate cancers, including those resistant to androgen deprivation or antiandrogen therapies. SIGNIFICANCE: Advanced prostate cancers resistant to androgen receptor antagonists are still susceptible to nontoxic BRD9 inhibitors, making them a promising alternative for halting AR signaling in progressed disease.

| S-EPMC8026650 | biostudies-literature

BRD9 is a regulator of androgen receptor signaling and prostate cancer progression - ChIP-Seq

Project description:BRD9 is a regulator of androgen receptor signaling and prostate cancer progression - ChIP-Seq

| PRJNA611536 | ENA

BRD9 is a regulator of androgen receptor signaling and prostate cancer progression - ChIP-Seq

Project description:BRD9 and BRD4 ChIP-Seq in LNCaP prostate cancer cells

2020-12-28 | GSE146623 | GEO

BRD9 is a critical regulator of androgen receptor signaling and prostate cancer progression - RNA-Seq

Project description:Standard RNA-Seq analysis from LNCaP cells treated with shBRD9 for 3d, shBRD9 for 11d, or 3 µM IBRD9 for 3d.

2020-12-28 | GSE146624 | GEO

The effects of enzalutamide on androgen-dependent and androgen-independent prostate cancer cells.

Project description:To investigate the mechanisms of drug resistance and castration resistance in prostate cancer, we performed proteomic sequencing on androgen-dependent prostate cancer cells (LNCaP) and androgen-independent cells (AI) treated with enzalutamide.

2024-11-26 | PXD058261 |

BRD9 is a regulator of androgen receptor signaling and prostate cancer progression

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

2020-12-28 | GSE146625 | GEO

Genome-wde mapping of BRD9 binding sites and gene expression changes upon BRD9 knockdown

Project description:Leukemia is characterized by genetic and epigenetic mutations resulting in selection of cancer cells, which are unable to differentiate. While genetic alterations are difficult to target, the epigenome is intrinsically dynamic and readily offers new therapeutic strategies. Thus, identifying cancer-specific context-dependent targets and unraveling their biological function may open up new therapeutic perspectives. Here, we identify bromodomain-containing protein 9 (BRD9) as a critical target required in acute myeloid leukemia (AML). We show that BRD9 is overexpressed in AML cells including ex vivo primary blasts compared to CD34+ cells. By targeting BRD9 expression in AML, we observed an alteration in proliferation and survival, ultimately resulting in the induction of apoptosis. Intriguingly, genome-wide profiling revealed that BRD9 binds enhancer regions in a cell type-specific manner, regulating cell type-related processes. We unveil a novel BRD9-sustained STAT5 pathway activation via regulation of SOCS3 expression levels. Our findings identify a previously undescribed BRD9-STAT5 axis as critical for leukemia maintenance, suggesting BRD9 as a potential therapeutic target.

2019-05-02 | GSE129437 | GEO

Kaiso, a critical regulator of spermatogenesis

Project description:Kaiso, a critical regulator of spermatogenesis

| PRJNA436947 | ENA

BRD9 regulates leukemic cell survival via STAT5 pathway inhibition

Project description:Leukemia is characterized by genetic and epigenetic mutations resulting in selection of cancer stem cells, which are unable to differentiate. While genetic alterations are difficult to target, the epigenome is intrinsically dynamic and readily offers new therapeutic strategies. Thus, identifying cancer-specific context-dependent targets and unraveling their biological function may open up new therapeutic perspectives. Here, we identify bromodomain-containing protein 9 (BRD9) as a critical target required in acute myeloid leukemia (AML). We show that BRD9 is overexpressed in AML cells including ex vivo primary blasts compared to CD34+. By targeting BRD9 expression in AML, we observed an alteration in proliferation and survival, ultimately resulting in the induction of apoptosis. Intriguingly, genome-wide profiling revealed that BRD9 binds enhancer regions in a cell type-specific manner, regulating cell type-related processes. We unveil a novel BRD9-sustained STAT5 pathway activation via regulation of SOC3 expression levels. Our findings identify a previously undescribed BRD9-STAT5 axis as critical for leukemia maintenance, suggesting BRD9 as a potential therapeutic target.

2019-11-11 | PXD013245 | Pride

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