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EP300/CREBBP acetyltransferase inhibition limits steroid receptor and FOXA1 signaling in prostate cancer cells

ABSTRACT: EP300/CREBBP acetyltransferase inhibition limits steroid receptor and FOXA1 signaling in prostate cancer cells

PROVIDER: PRJNA1030770 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26458200_1.fastq.gz	Fastqsanger.gz
	SRR26458200_2.fastq.gz	Fastqsanger.gz
	SRR26458300.fastq.gz	Fastqsanger.gz
	SRR26458201_1.fastq.gz	Fastqsanger.gz
	SRR26458201_2.fastq.gz	Fastqsanger.gz

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EP300/CREBBP acetyltransferase inhibition limits steroid receptor and FOXA1 signaling in prostate cancer cells (RNA-seq)

Project description:The androgen receptor (AR) serves as the primary target for therapeutic intervention in prostate cancer (PCa), and AR-targeted treatments constitute the cornerstone of clinical management for this malignancy. Nevertheless, their effectiveness is often compromised by the emergence of resistance mechanisms. These resistant forms of PCa persist in activating AR signaling, highlighting the urgent need for new therapeutic strategies to combat therapy-resistant PCa. Resistance to AR-targeted therapies can manifest through a multitude of mechanisms, including the overexpression of AR splice variants and altered activities of other transcription factors, such as the glucocorticoid receptor (GR) and FOXA1. A shared characteristic among these transcription factors is their dependence on a common set of coregulators, with EP300/CREBBP being a prominent example. This suggests a compelling rationale for employing coregulatory-targeted therapies in the management of treatment-resistant PCa. Here, we aimed to explore the impact of EP300/CREBBP acetyltransferase inhibition on steroid receptor and FOXA1 signaling in PCa cells, employing genome-wide techniques. Our findings illuminate that EP300/CREBBP inhibition exerts a substantial disruptive effect on the AR-regulated transcriptome and receptor chromatin binding, primarily by downregulating the AR-gene. Similarly, the transcriptome regulated by GR and the chromatin binding of the receptor were also hindered, although this was not associated with decreased GR expression levels. Instead, EP300/CREBBP acetyltransferase inhibition leads to a significant reduction in FOXA1 chromatin binding, consequently constraining GR signaling. In summary, our results emphasize how EP300/CREBBP acetyltransferase inhibition distinctly curtails the signaling activities of oncogenic transcription factors, underscoring the potential effectiveness of coregulatory-targeted therapies in PCa.

2024-03-14 | GSE245968 | GEO

EP300/CREBBP acetyltransferase inhibition limits steroid receptor and FOXA1 signaling in prostate cancer cells (ChIP-seq)

2024-03-14 | GSE245967 | GEO

EP300/CREBBP acetyltransferase inhibition limits steroid receptor and FOXA1 signaling in prostate cancer cells (ATAC-seq)

2024-03-14 | GSE245966 | GEO

EP300/CREBBP acetyltransferase inhibition limits steroid receptor and FOXA1 signaling in prostate cancer cells (ChIP-seq)

Project description:EP300/CREBBP acetyltransferase inhibition limits steroid receptor and FOXA1 signaling in prostate cancer cells (ChIP-seq)

| PRJNA1030765 | ENA

EP300/CREBBP acetyltransferase inhibition limits steroid receptor and FOXA1 signaling in prostate cancer cells (RNA-seq)

Project description:EP300/CREBBP acetyltransferase inhibition limits steroid receptor and FOXA1 signaling in prostate cancer cells (RNA-seq)

| PRJNA1030766 | ENA

EP300/CREBBP acetyltransferase inhibition limits steroid receptor and FOXA1 signaling in prostate cancer cells (ATAC-seq)

Project description:EP300/CREBBP acetyltransferase inhibition limits steroid receptor and FOXA1 signaling in prostate cancer cells (ATAC-seq)

| PRJNA1030764 | ENA

EP300/CREBBP acetyltransferase inhibition limits steroid receptor and FOXA1 signaling in prostate cancer cells.

Project description:The androgen receptor (AR) is a primary target for treating prostate cancer (PCa), forming the bedrock of its clinical management. Despite their efficacy, resistance often hampers AR-targeted therapies, necessitating new strategies against therapy-resistant PCa. These resistances involve various mechanisms, including AR splice variant overexpression and altered activities of transcription factors like the glucocorticoid receptor (GR) and FOXA1. These factors rely on common coregulators, such as EP300/CREBBP, suggesting a rationale for coregulator-targeted therapies. Our study explores EP300/CREBBP acetyltransferase inhibition's impact on steroid receptor and FOXA1 signaling in PCa cells using genome-wide techniques. Results reveal that EP300/CREBBP inhibition significantly disrupts the AR-regulated transcriptome and receptor chromatin binding by reducing the AR-gene expression. Similarly, GR's regulated transcriptome and receptor binding were hindered, not linked to reduced GR expression but to diminished FOXA1 chromatin binding, restricting GR signaling. Overall, our findings highlight how EP300/CREBBP inhibition distinctively curtails oncogenic transcription factors' signaling, suggesting the potential of coregulatory-targeted therapies in PCa.

| S-EPMC10987371 | biostudies-literature

CREBBP/EP300 acetyltransferase inhibition targets lineage specific enhancers to inhibit the proliferation of ER+ breast cancer cells [ATAC-Seq]

Project description:MCF7 cells were treated with a CREBBP/EP300 acetyltransferase inhibitor CPI-1612 and chromatin status was measured via ATAC-seq

2022-03-04 | GSE190159 | GEO

CREBBP/EP300 acetyltransferase inhibition targets lineage specific enhancers to inhibit the proliferation of ER+ breast cancer cells [scATAC-Seq]

Project description:MCF7 cells were treated with a CREBBP/EP300 acetyltransferase inhibitor CPI-1612 and chromatin status was measured via single-cell ATAC-seq

2022-03-04 | GSE190162 | GEO

CREBBP/EP300 acetyltransferase inhibition targets lineage specific enhancers to inhibit the proliferation of ER+ breast cancer cells [ChIP-Seq]

Project description:MCF7 were treated with a CREBBP/EP300 acetyltransferase inhibitor CPI-1612 or DMSO and ChIP-seq was performed for H3K27ac and H3K9ac.

2022-03-04 | GSE190161 | GEO

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