Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Targeting FOXA1-mediated repression of TGF-β signaling suppresses castration-resistant prostate cancer progression [microarray]

ABSTRACT: our study establishes FOXA1 as an important regulator of lineage plasticity mediated in part by TGF-β signaling and supports a novel therapeutic strategy to control lineage switching and potentially extend clinical response to antiandrogen therapies.

ORGANISM(S): Homo sapiens

PROVIDER: GSE119758 | GEO | 2018/11/01

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Targeting FOXA1-mediated repression of TGF-β signaling suppresses castration-resistant prostate cancer progression [RNA-Seq]

Project description:our study establishes FOXA1 as an important regulator of lineage plasticity mediated in part by TGF-β signaling and supports a novel therapeutic strategy to control lineage switching and potentially extend clinical response to antiandrogen therapies.

2018-11-01 | GSE119757 | GEO

Targeting FOXA1-mediated repression of TGF-? signaling suppresses castration-resistant prostate cancer progression.

Project description: Not available

| S-EPMC6355239 | biostudies-literature

Targeting FOXA1-mediated repression of TGF-β signaling suppresses castration-resistant prostate cancer progression

Project description:Targeting FOXA1-mediated repression of TGF-β signaling suppresses castration-resistant prostate cancer progression

| PRJNA490185 | ENA

Targeting FOXA1-mediated repression of TGF-β signaling suppresses castration-resistant prostate cancer progression

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

2018-11-01 | GSE119759 | GEO

Targeting FOXA1-mediated repression of TGF-β signaling suppresses castration-resistant prostate cancer progression [microarray]

Project description:Targeting FOXA1-mediated repression of TGF-β signaling suppresses castration-resistant prostate cancer progression [microarray]

| PRJNA490187 | ENA

Nucleation of DNA Repair Factors by FOXA1 Links DNA Demethylation and Transcriptional Pioneering

Project description:We report that the winged helix transcription factor FOXA1 is unexpectedly associated with components of single and double stranded-DNA repair complexes. Biochemical studies and high-throughput approaches validated the hierarchical composition of this FOXA1-nucleated machinery and revealed the dependency on FOXA1 for global targeting of the key repair polymerase POLB. Genome-wide DNA methylomes at single-base resolution demonstrated that FOXA1-DNA repair complex is functionally linked to DNA demethylation in a lineage specific fashion. Loss-of-function studies indicate that a significant portion of FOXA1-bound regions display localized reestablishment of methylation and that the subsets with most consistent hypermethylation are represented by active promoters and enhancers that also exhibit the greatest depletion of POLB following FOXA1 removal. Consistently, forced expression of FOXA1 commits its binding sites to an active DNA demethylation in a POLB dependent manner. Finally, we showed that FOXA1-associated DNA demethylation is tightly coupled with genomic targeting of estrogen receptor and estrogen responsiveness. Together, our results link FOXA1-associated DNA demethylation to its transcriptional pioneering.

2016-06-08 | PXD004271 | Pride

Targeting FOXA1-mediated repression of TGF-β signaling suppresses castration-resistant prostate cancer progression [RNA-Seq]

Project description:Targeting FOXA1-mediated repression of TGF-β signaling suppresses castration-resistant prostate cancer progression [RNA-Seq]

| PRJNA490188 | ENA

Chromatin accessibility and pioneer factor FOXA1 restrict glucocorticoid receptor action in prostate cancer (RNA-Seq)

Project description:Treatment of prostate cancer relies predominantly on the inhibition of androgen receptor (AR) signaling. Despite the initial effectiveness of the AR-targeted therapies, the cancer often develops resistance to the AR blockade. One mechanism of the resistance is glucocorticoid receptor (GR)-mediated replacement of AR. Nevertheless, the mechanistic ways and means how the GR-mediated antiandrogen resistance occurs has remained elusive. Here, we have discovered several crucial features of GR action in prostate cancer cells through genome-wide techniques. We detected that the replacement of AR by GR in antiandrogen-exposed prostate cancer cells occurs almost exclusively at pre-accessible chromatin sites displaying FOXA1 occupancy. Counterintuitively to the classical pioneer factor model, silencing of FOXA1 potentiated the chromatin binding and transcriptional activity of GR. This was attributed to FOXA1-mediated repression of the NR3C1 (gene encoding GR) expression via the corepressor TLE3. In comparison to FOXA1, inhibition of coregulator activity efficiently restricted GR-mediated gene regulation and cell proliferation. Overall, we identified chromatin pre-accessibility and FOXA1-mediated repression as important regulators of GR action in prostate cancer, pointing out new avenues to oppose steroid receptor-mediated drug resistance.

2023-11-07 | GSE214756 | GEO

Chromatin accessibility and pioneer factor FOXA1 restrict glucocorticoid receptor action in prostate cancer (ChIP-Seq)

2023-11-07 | GSE214754 | GEO

Chromatin accessibility and pioneer factor FOXA1 restrict glucocorticoid receptor action in prostate cancer (ATAC-Seq)

2023-11-07 | GSE214753 | GEO