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

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

PROVIDER: PRJNA887026 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21800600.fastq.gz	Fastqsanger.gz
	SRR21800601.fastq.gz	Fastqsanger.gz
	SRR21800602.fastq.gz	Fastqsanger.gz
	SRR21800603.fastq.gz	Fastqsanger.gz
	SRR21800604.fastq.gz	Fastqsanger.gz

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Chromatin accessibility and pioneer factor FOXA1 restrict glucocorticoid receptor action in prostate cancer

Project description:Chromatin accessibility and pioneer factor FOXA1 restrict glucocorticoid receptor action in prostate cancer

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

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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.

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

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

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Chromatin accessibility and pioneer factor FOXA1 restrict glucocorticoid receptor action in prostate cancer.

Project description:Treatment of prostate cancer relies predominantly on the inhibition of androgen receptor (AR) signaling. Despite the initial effectiveness of the antiandrogen therapies, the cancer often develops resistance to the AR blockade. One mechanism of the resistance is glucocorticoid receptor (GR)-mediated replacement of AR function. Nevertheless, the mechanistic ways and means how the GR-mediated antiandrogen resistance occurs have 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 enzalutamide-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. Moreover, the small-molecule inhibition of coactivator p300's enzymatic 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 antiandrogen resistance.

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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

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Chromatin accessibility and pioneer factor FOXA1 restrict glucocorticoid receptor action in prostate cancer

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

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