← BioTransfer GEO Dataset Finder
GEO series

BRD2 Bromodomain-Mediated Regulation of Cell State Plasticity Modulates Therapy Response in Glioblastoma

GSE304029 Mus musculus (mouse) RNA-seq (gene expression) 56 samples Submitted 2025/11/17 Platform GPL24676Platform GPL34284Platform GPL34290
At a glance

RNA-seq (gene expression) · mouse · 56 samples

What it is
RNA-seq (gene expression)Gene activity measured by sequencing. The summary does not mention single-cell work, so this is most likely bulk: one average per sample, the usual starting point for comparing groups.
Organism
Mus musculus (mouse)
Topic
GlioblastomaThis series is part of our curated briefing on it.
Samples
56 samples: 19 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
BRD2 bromodomain-mediated regulation of cell state plasticity modulates therapy response in glioblastomaNeuro-oncology · 2025
Summary (written by the submitters)
Background: Glioblastoma (GBM) displays remarkable cell state plasticity, a major contributor to therapeutic resistance and tumor progression. While epigenetic mechanisms play a central role in driving this plasticity, the key regulators remain poorly understood, and developing effective therapeutic strategies targeting them has been challenging.
Read the full summary ↓
Methods: We investigated the role of BRD2, a key regulator of NF-κB mediated mesenchymal (MES) transition, using GBM patient-derived xenograft (PDX) cell lines, CRISPR-mediated knock-in/knockout approaches, RNA-seq, and in vitro and in vivo modeling. BET inhibitors were employed to target MES gene expression and sensitize GBM to radiation therapy. Results: We found that PTEN loss induces RelA chromatin localization and acetylation-mediated recruitment of BRD2 to the MES gene promoters. BRD2 binding is essential for maintaining MES gene expression and phenotype. Genetic ablation or loss-of-function mutation of BRD2 bromodomains reverses MES transition, enhances radiation sensitivity, and improves survival in orthotopic xenograft models. Additionally, treatment with a brain-penetrant BD2-selective inhibitor suppresses the MES phenotype and increases radiation sensitivity of GBM stem cells in vitro. Conclusion: Our study identifies BRD2 as a key mediator of MES transition in GBM, with its bromodomains playing a crucial role in driving cell state plasticity. Targeting BRD2 with BD2-selective inhibitors offers a promising therapeutic strategy to overcome radiation resistance and improve outcomes for GBM patients.
Published in
BRD2 bromodomain-mediated regulation of cell state plasticity modulates therapy response in glioblastoma
Vadla R, Taylor B, Miyake Y et al. · Neuro-oncology 2025 · PMID 40686478 · doi:10.1093/neuonc/noaf169
This dataset
Open GSE304029 in finder → Find more RNA-seq datasets → Glioblastoma landscape →
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 GSE304029_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: For RNA-seq the counts are usually a table among the supplementary files (look for 'counts', 'expression', 'FPKM' or 'TPM' in the file name). The series matrix of a sequencing study is sometimes nearly empty.

Also filed as BioProject PRJNA1298802 and SRA study SRP604626. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 40686478) ↗
Study design
19 conditions, mostly in triplicate
GSC11 cells, shControl ×3 GSC11 cells, shBRD2 ×3 GSC11 cells, RelA K310 ×3 GSC11 cells, BRD2_WT ×3 GSC11 cells, BRD2_BD1 ×3 GSC11 cells, BRD2_BD2 ×3 GSC11 cells, BRD2_BD1/2 ×3 TS576 cell, PTENKO ×3 +12 more

Supports a between-group comparison across 55 samples.

How we read this: 19 replicated groups read from 56 sample titles; they account for 55 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

+ 16 more — browse all 56 samples with per-sample file links →

More Glioblastoma datasets

Search all RNA-seq datasets in GEO →

Share this dataset

Metadata from NCBI GEO, cached and refreshed periodically — the NCBI page above is authoritative. Downloads link straight to NCBI/ENA; nothing is proxied through BioTransfer.