Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Altered chromatin remodeling by FOXA1 mutations promotes androgen independence and prostate cancer aggressiveness [gene expression]

ABSTRACT: FKHD-mutant (FKHDm) FOXA1 has impaired ability to bind chromatin and thus failed to rescue wildtype FOXA1-mediated transcriptional program. FKHDm FOXA1 formed much stronger interaction with the AR protein, thereby preventing AR from binding to the chromatin.

ORGANISM(S): Homo sapiens

PROVIDER: GSE128882 | GEO | 2019/11/21

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Altered chromatin remodeling by FOXA1 mutations promotes androgen independence and prostate cancer aggressiveness [ChIP-seq]

Project description:FKHD-mutant (FKHDm) FOXA1 has impaired ability to bind chromatin and thus failed to rescue wildtype FOXA1-mediated transcriptional program. FKHDm FOXA1 formed much stronger interaction with the AR protein, thereby preventing AR from binding to the chromatin.

2019-11-21 | GSE128883 | GEO

FOXA1 ChIP-seq in LNCaP cell line overexpressing WT or mutant FOXA1

Project description:Our data suggested that FKHD-MSs impair the chromatin binding of FOXA1 to AR-dependent enhancers and thus suppress AR transcriptional activity, and promote PCa progression through increasing FOXA1 binding to a subset of AR-independent enhancers that regulates transcription of genes mediating EMT and metastasis

2019-10-15 | GSE133386 | GEO

RNA-seq in LNCaP cell line overexpressing WT or mutant FOXA1

2019-10-15 | GSE133384 | GEO

H3K27ac ChIP-seq in LNCaP cell line overexpressing WT or mutant FOXA1

2019-10-15 | GSE133387 | GEO

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

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. genetic_modification_design

2016-01-11 | E-GEOD-69044 | biostudies-arrayexpress

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

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

Drug-induced epigenomic plasticity reprograms circadian rhythm regulation to drive prostate cancer towards androgen-independence

Project description:In prostate cancer, androgen receptor (AR)-targeting agents are very effective in various stages of the disease. However, therapy resistance inevitably occurs and little is known about how tumor cells adapt to bypass AR suppression. Here, we performed integrative multi-omics analyses on tissues isolated before and after 3 months of AR-targeting enzalutamide monotherapy from high-risk prostate cancer patients enrolled in a neoadjuvant clinical trial. Transcriptomic analyses demonstrated that AR inhibition drove tumors towards a neuroendocrine-like disease state. In addition, epigenomic profiling revealed massive enzalutamide-induced reprogramming of pioneer factor FOXA1 – from inactive chromatin binding sites towards active cis-regulatory elements that dictate pro-survival signals. Notably, treatment-induced FOXA1 sites were enriched for the circadian rhythm core component ARNTL. Post-treatment ARNTL levels associated with poor outcome, and ARNTL suppression decreased cell growth in vitro. Our data highlight a remarkable cistromic plasticity of FOXA1 following AR-targeted therapy, and revealed an acquired dependency on circadian regulator ARNTL, a novel candidate therapeutic target.

2022-10-14 | PXD032041 | Pride

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

2016-01-11 | GSE69044 | GEO

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

2016-01-11 | GSE69043 | GEO

FoxA1 inhibits androgen receptor expression and suppresses prostate cancer metastasis [DU145, 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. ChIP-Seq examination of AR and FoxA1 binding sites, FAIRE-seq detection of open chromatin genomic regions in DU145 AR +/- FOXA1 cells

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

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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