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Specific cPRC1 complexes are co-opted to mediate oncogenic gene repression in diffuse midline glioma

GSE246931 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 164 samples Submitted 2025/05/28 Platform GPL34284Platform GPL18573
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 164 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
164 samples: 59 conditions, mostly in triplicateGroups 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
A specific form of cPRC1 containing CBX4 is co-opted to mediate oncogenic gene repression in diffuse midline gliomaMolecular cell · 2025
Summary (written by the submitters)
Diffuse midline glioma (DMG) is a fatal childhood brain tumour characterised primarily by mutant histone H3 (H3K27M). H3K27M causes a global reduction in Polycomb Repressive Complex 2 (PRC2)-mediated H3K27me3 by inhibiting PRC2 enzymatic activity. Paradoxically, PRC2 is essential in DMG tumour cells where residual complex activity is required for oncogenic gene repression, although the molecular mechanisms acting downstream of PRC2 in this context are poorly understood.
Read the full summary ↓
Here, we’ve discovered this oncogenic gene repression is mediated by specific canonical PRC1 (cPRC1) formations. By combining CRISPR screening, biochemical and chromatin mapping approaches with functional perturbations we show that cPRC1 complexes containing CBX4 and PCGF4 drive oncogenic gene repression downstream of H3K27me3 in DMG cells. Remarkably, the altered H3K27me3 modification landscape characteristic of these tumours rewires the distribution of cPRC1 complexes on chromatin. CBX4 and PCGF4 containing cPRC1 accumulate at sites of H3K27me3 while other cPRC1 formations are displaced. Despite accounting for <5% of cPRC1 complexes in DMG, CBX4/PCGF4-containing complexes predominate as gene repressors. Our findings link the altered distribution of H3K27me3 with imbalanced cPRC1 function, promoting oncogenic gene repression in DMG cells, revealing new disease mechanisms and highlighting potential therapeutic opportunities in this incurable childhood brain tumour.
Published in
A specific form of cPRC1 containing CBX4 is co-opted to mediate oncogenic gene repression in diffuse midline glioma
Lagan E, Gannon D, Silva AJ et al. · Molecular cell 2025 · PMID 40403727 · doi:10.1016/j.molcel.2025.04.026
This dataset
Open GSE246931 in finder → Find more human RNA-seq datasets →
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.

Series matrix ↓
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 GSE246931_RAW.tar (it can run to tens of gigabytes).

All supplementary files ↗ Whole study · RAW.tar ↓
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.

Raw reads on ENA ↗

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 PRJNA1035121 and SRA study SRP469978. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 40403727) ↗
Study design
59 conditions, mostly in triplicate
Quantseq_K27M_DMSO_Day3 ×3 Quantseq_K27M_DMSO_Day6 ×3 Quantseq_K27M_DMSO_Day9 ×3 Quantseq_K27M_TAZ_Day3 ×3 Quantseq_K27M_TAZ_Day6 ×3 Quantseq_K27M_TAZ_Day9 ×3 Quantseq_KO_Day3 ×3 K27M-BMI1 ×3 +52 more

Supports a case/control comparison: 6 samples read as cases, 28 as controls.

How we read this: 59 replicated groups read from 164 sample titles; they account for 163 of them. 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

+ 124 more — browse all 164 samples with per-sample file links →

Datasets on a similar topic

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