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Targeting histone H2B acetylated enhanceosomes via p300/CBP degradation in prostate cancer (ChIP-Seq)

GSE255132 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 38 samples Submitted 2025/06/26 Platform GPL24676Platform GPL16791
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 38 samples

What it is
ChIP-seq / ATAC-seq (genome binding and open chromatin)Where proteins bind the genome, or which regions are open and active.
Organism
Homo sapiens (human)
Samples
38 samples: 37 distinct titles, 1 of them repeatedGroups are read from the sample names, not from the paper. Check the list below.
Data you can get
A processed table (series matrix) and supplementary files from NCBI; the raw sequencing reads from ENA. Which of these hold counts depends on the study, so check the file list.
Paper
Targeting histone H2B acetylated enhanceosomes via p300/CBP degradation in prostate cancerNature genetics · 2025
Summary (written by the submitters)
Prostate cancer (PCa) is driven by oncogenic transcription factor enhanceosomes comprising chromatin and epigenetic regulators. The lysine acetyltransferases p300 and CBP are key cofactors that activate enhancers through histone acetylation. Here, we identify p300/CBP-mediated multisite acetylation of the histone H2B N-terminus (H2BNTac) as a defining feature of oncogenic enhanceosomes in androgen receptor (AR)-positive prostate cancerPCa.
Read the full summary ↓
p300/CBP are essential for AR and ERG transcriptional activity, and their dual degradation eliminates H2BNTac and H3K27ac marks at hyperactive enhancers, leading to stronger suppression of oncogenic transcription more effectively than targeting either paralog or bromodomains alone. Cytotoxicity profiling across >900 cell lines revealed that tumors with high H2BNTac, including AR-positive prostate cancerPCa, are selectively dependent on p300/CBP. In preclinical models, systemic p300/CBP degradation inhibited tumor growth, synergized with AR antagonists, and showed no evident toxicity. These findings position H2BNTac as an key epigenetic marker of enhancer addiction and establish support dual p300/CBP degradation as a promising therapeutic strategypy for enhancer-driven cancers.
Published in
Targeting histone H2B acetylated enhanceosomes via p300/CBP degradation in prostate cancer
Luo J, Chen Z, Qiao Y et al. · Nature genetics 2025 · PMID 41044247 · doi:10.1038/s41588-025-02336-6
This dataset
Download · which file do I need?

Direct links to NCBI and ENA, no account and no request form. Pick by what you want to do: take the small processed table to look, the supplementary files to re-analyse, or the original raw data to start over.

1 · Just have a look

Processed table

The series matrix: one table of values per sample as the submitters processed it. The smallest download, and it opens in Excel or R. Start here to see what the data look like.

2 · Re-analyse it

Supplementary files

The count tables and other files the authors uploaded. Take only the samples you need, or the whole study as GSE255132_RAW.tar (it can run to tens of gigabytes).

3 · Start from the raw reads

Raw sequencing reads

The original FASTQ files, straight from the sequencer, held at ENA. Large, and you align them yourself, so only choose this if you need to re-process the study from scratch.

What the files usually look like: Look for peak files (.bed, .narrowPeak) and signal tracks (.bigWig) among the supplementary files; the raw reads are on ENA.

Also filed as BioProject PRJNA1073576 and SRA study SRP488340. Searching any of these in the dataset finder brings you back here.

Study design
37 distinct titles, 1 of them repeated
VCaP_DMSO_BRD ×2

How we read this: Read from 38 sample titles: 37 distinct titles with little repetition. These groups are guessed from the sample names, not taken from the paper, so check them against the sample list below before relying on them.

Samples in this study
Datasets on a similar topic

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