Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

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

ABSTRACT: 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

ORGANISM(S): Homo sapiens

PROVIDER: GSE133386 | GEO | 2019/10/15

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

RNA-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 | GSE133384 | GEO

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

2019-10-15 | GSE133387 | GEO

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

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

2019-11-21 | GSE128882 | GEO

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

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

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

Genome-wide occupation of AR, FOXA1, and H3K27AC in LNCaP cells treated with selective PARP2 inhibitor UPF-1069

Project description:Androgen receptor (AR) signaling is a key driver of prostate cancer (PCa) growth and progression. Understanding the factors influencing AR-mediated transcription provides new opportunities for therapeutic intervention. We have previously discovered that a genetic variant in one of the DNA repair genes, PARP2, is associated with aggressive PCa. Here, we show that a high expression level of PARP2 in PCa tumors is associated with high Gleason scores and biochemical recurrence using The Cancer Genome Atlas (TCGA) dataset. Functional studies reveal that PARP2 enhances AR-mediated gene expression through interacting with the pioneer factor FOXA1 and facilitating AR recruitment to the enhancer regions genome-wide in PCa cells. Selective targeting of PARP2, but not PARP1, by genetic or pharmacological means blocks interaction between PARP2 and FOXA1, which in turn attenuates AR-mediated transcription and inhibits AR-positive PCa growth. SIGNIFICANCE: Current anti-androgens act through blocking ligand binding or inhibiting androgen synthesis. Selective targeting of PARP2 may provide a novel therapeutic approach for AR inhibition by disruption of FOXA1 function, which may be beneficial to patients, irrespective of their DNA repair defect status and, more importantly, when direct AR-targeted therapies fail.

2019-06-24 | GSE114274 | GEO

FOXA1 potentiates lineage-specific enhancer activation through modulating TET1 expression and function

Project description:FOXA1 is a FKHD family protein that translates epigenetic signatures at target enhancers to lineage-specific transcription and differentiation. Through genome-wide location analyses, here we show that FOXA1 expression and occupancy are, in turn, required for the maintenance of this epigenetic signature, namely DNA hypomethylation and histone 3 lysine 4 methylation. Mechanistically, this involves TET1, a 5-methylcytosine dioxygenase. We found that FOXA1 induces TET1 expression via direct binding at its cis-regulatory elements. Further, FOXA1 physically interacts with the TET1 protein through its CXXC domain. TET1 thus co-occupies FOXA1-dependent enhancers and mediates local DNA demethylation and concomitant histone 3 lysine 4 methylation, further potentiating FOXA1 recruitment. FOXA1 binding events were markedly reduced following TET1 depletion. Together, our results support that FOXA1 is not only a reader, but also a writer, of the epigenetic signatures at lineage-specific enhancers and that TET1 and FOXA1 form a feed-forward regulatory loop for enhancer activation. ChIP-Seq examination of FOXA1 binding sites in LNCaP cell, and epigenetic markers (5mC, 5hmC, H3K4me2) profiling upon TET1 depletion

2016-07-22 | E-GEOD-73363 | 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 [gene expression]

2016-01-11 | GSE69044 | GEO

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