Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Cooperativity and Equilibrium with FOXA1 Define Androgen Receptor Transcriptional Program [array]

ABSTRACT: Previous studies have shown that FOXA1 defines prostatic AR binding events, the underlying mechanisms of which, however, are incompletely understood.

ORGANISM(S): Homo sapiens

PROVIDER: GSE54991 | GEO | 2014/06/02

SECONDARY ACCESSION(S): PRJNA238217

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Cooperativity and Equilibrium with FOXA1 Define Androgen Receptor Transcriptional Program [array]

Project description:Previous studies have shown that FOXA1 defines prostatic AR binding events, the underlying mechanisms of which, however, are incompletely understood. To test whether ectopic AR and FOXA1 can activate AR target genes, we performed adenoviral of LacZ, AR, FOXA1 or AR+FOXA1 proteins in DU145 cells, followed by microarray analysis of these cells.

2014-06-02 | E-GEOD-54991 | biostudies-arrayexpress

Cooperativity and equilibrium with FOXA1 define the androgen receptor transcriptional program.

Project description:The pioneering factor FOXA1 opens chromatin to facilitate androgen receptor (AR) binding to prostate-specific genes. How FOXA1 controls the AR cistrome, however, is incompletely understood. Here we show that AR directly binds chromatin through the androgen response elements (AREs). FOXA1 is not required for AR-chromatin interaction, but instrumental in recruiting AR to low-affinity half-AREs by opening local chromatin around adjacent FKHD sites. Too much FOXA1 creates excessive open chromatin regions, which serve as reservoirs that retain AR via abundant half-AREs, thereby reducing its availability for specific sites. FOXA1 downregulation, by contrast, relinquishes AR to permissively bind AREs across the genome, resulting in substantial AR-binding events and AR target gene expression even in the absence of androgen. Taken together, our data illustrate the mechanistic details by which cooperativity and equilibrium with FOXA1 define AR cistrome and reveal a previously unknown function of FOXA1 in inhibiting AR signalling and castration-resistant prostate cancer growth.

| S-EPMC4088269 | biostudies-literature

Cooperativity and Equilibrium with FOXA1 Define Androgen Receptor Transcriptional Program

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2014-06-02 | E-GEOD-55007 | biostudies-arrayexpress

Cooperativity and Equilibrium with FOXA1 Define Androgen Receptor Transcriptional Program

Project description:Cooperativity and Equilibrium with FOXA1 Define Androgen Receptor Transcriptional Program

| PRJNA238234 | ENA

Cooperativity and Equilibrium with FOXA1 Define Androgen Receptor Transcriptional Program

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

2014-06-02 | GSE55007 | GEO

Androgen receptor-independent function of FoxA1 in prostate cancer metastasis

Project description:FoxA1 has been shown critical for prostate development and prostate-specific gene expression regulation. In addition to its well-established role as an AR pioneering factor,several studies have recently revealed significant AR binding events in prostate cancer cells with FoxA1 knockdown. Furthermore, the role of FoxA1 itself in prostate cancer has not been carefully examined. Thus, it is important to understand the role of FoxA1 in prostate cancer and how it interacts with AR signaling. To address these questions, we generated engineered LNCaP cells with FoxA1 knockdown using shRNA or siRNA, 22RV1 cells with stable FoxA1 knockdown and PC3M cells with FoxA1 stable overexpression. We performed microarray analysis of these cells. We performed microarray analysis on LNCaP cells with FoxA1 knockdown using shRNA or siRNA, 22RV1 cells with stable FoxA1 knockdown and PC3M cells with FoxA1 stable overexpression

2013-04-05 | E-GEOD-37314 | biostudies-arrayexpress

FoxA1 inhibits androgen receptor expression and suppresses prostate cancer metastasis [DU145, ChIP-seq]

2014-06-02 | E-GEOD-47987 | biostudies-arrayexpress

FoxA1 inhibits androgen receptor expression and suppresses prostate cancer metastasis [LNCaP, ChIP-seq]

Project description:FoxA1 has been shown critical for prostate development and prostate-specific gene expression regulation. In addition to its well-established role as an AR pioneering factor,several studies have recently revealed significant AR binding events in prostate cancer cells with FoxA1 knockdown. Furthermore, the role of FoxA1 itself in prostate cancer has not been carefully examined. Thus, it is important to understand the role of FoxA1 in prostate cancer and how it interacts with AR signaling. To address these questions, we generated LNCaP cells with stable FoxA1 knockdown. We performed AR/FoxA1 ChIP-seq and microarray analysis of these cells. ChIP_Seq examination of AR and FoxA1 binding sites in LNCaP shCtrl and shFoxA1 cells

2014-06-02 | E-GEOD-37345 | biostudies-arrayexpress

Pioneer factor FOXA1 defines GATA2- and AR-mediated transcriptional program in prostate cancer [ChIP-Seq]

Project description:AR is tightly regulated by many transcriptional cofactors, including key pioneer factor such as FOXA1 and GATA2. While FOXA1 was recently shown to be able to redistribute AR across the genome, how GATA2 regulates AR cistrome has not been carefully investigated. Here, we report that, unlike FOXA1, GATA2 is unable to reprogram AR, but instead it enhances AR program by inducing AR expression and augmenting AR co-occupancy, thereby acting as a pure AR coactivator, rather than a pioneer factor. On the other hand, AR co-occupancy enhances both GATA2 and FOXA1 binding on the chromatin, forming a positive feedback loop. Importantly, we found that FOXA1 is also capable of reprogramming GATA2 by recruiting GATA2 from GATA motif to FKHD-containing regions, being analogous to its pioneering effect on AR signaling. By contrast, GATA2 simply acts as a co-activator of FOXA1 with a lack of pioneering ability. ChIP_Seq examination of AR, FoxA1 and GATA2 binding sites in LNCaP and DU145 cells

2016-01-11 | E-GEOD-69043 | biostudies-arrayexpress

The role of the transcription factors GATA2 and FOXA1 in immortalized basal-like prostate epithelial cells

Project description:GATA2 and FOXA1 are pioneering factors for Androgen Receptor (AR) in prostate cancer cells. Less is known about their role in benign epithelial prostate cells. We investigated if they had the ability to induce differentiation in an undifferentiated prostatic context. Benign basal-like prostate epithelial cells 957E/hTERT-AR cells (a gift from John T. Isaacs lab, Johns Hopkins, MD, USA) were transduced with LentiORF RFP control lentiviral particles. The 957E/hTERT-AR-RFP cells were then transduced with GATA2 and FOXA1 lentiviral particles, and we called the new cell lines hTERT/AR-GATA2 and hTERT/AR-FOXA1, respectively. hTERT/AR-GATA2 is a stable selected cell line and treated with 1 nM anabolic steroids, R1881, or ethanol (ET-OH) for 48 hrs. 957E/hTERT/AR-FOXA1 is a transient cell line, because FOXA1 protein is quickly lost. Twenty four hours post transduction with FOXA1 lentivral particles, 1 nM androgen R1881 or ethanol (ET-OH) were added at time for medium exchange and further treated for 24 hours. GATA-2 and FOXA1 ability to induce differentiation was assessed.

2018-12-01 | E-MTAB-5121 | biostudies-arrayexpress

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