← BioTransfer GEO Dataset Finder
GEO series

Mediator Subunit MED4 Enforces Metastatic Dormancy in Breast Cancer (Histone ChIP-seq_shMed4)

GSE275130 Mus musculus (mouse) ChIP-seq / ATAC-seq (genome binding and open chromatin) 36 samples Submitted 2026/04/18 Platform GPL23479
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · mouse · 36 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
Mus musculus (mouse)
Samples
36 samples: 18 conditions, mostly in duplicateGroups 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
Mediator subunit MED4 enforces metastatic dormancy in breast cancerNature cell biology · 2026
Summary (written by the submitters)
Breast cancer metastatic relapse after a latency period, known as metastatic dormancy, involves dormant tumor cells within pre-metastatic niches. Through rigorous genetic screening in mice, we identified the mediator complex subunit 4 gene, Med4, as a novel tumor-cell intrinsic gatekeeper in metastatic reactivation. Med4 downregulation effectively awakened dormant breast cancer cells, prompting reactivation and macroscopic metastatic outgrowth in the lungs.
Read the full summary ↓
Med4 depletion results in profound changes in nuclear size and three-dimensional (3D) chromatin architecture from compacted to relaxed states in contrast to the known canonical function of the Mediator complex. These changes rewire the expression of extracellular matrix (ECM) proteins, integrins, and signaling components resulting in integrin-mediated mechano-transduction and activation of YAP and MRTF. In parallel, assembly of stress fibers pulls on the nuclear membrane, and thereby contributes to mediating and reinforcing the overall chromatin modifications that occur subsequent to Med4 depletion. MED4 gene deletions were observed in patients with metastatic breast cancer, and reduced MED4 expression correlates with worse prognosis. Our findings unveil a unique function of MED4 and identify an innovative mechanism by which MED4 regulates the epigenetic control of integrin signaling, pivotal in the metastatic reactivation of breast cancer. Additionally, we propose MED4 and related gene signatures as novel biomarkers for stratifying patients prone to recurrence, thus identifying subsets of patients who will benefit from targeting effectors activated by MED4 loss.
Published in
Mediator subunit MED4 enforces metastatic dormancy in breast cancer
Bae SS, Ling HH, Zhang J et al. · Nature cell biology 2026 · PMID 42332201 · doi:10.1038/s41556-026-01984-y
This dataset
Open GSE275130 in finder → Find more mouse ChIP / ATAC / CUT&Tag 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 GSE275130_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 PRJNA1149660 and SRA study SRP527279. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 42332201) ↗
Study design
18 conditions, mostly in duplicate
NTC H3K4me1 biol ×2 NTC H3K4me3 biol ×2 NTC H3K9me3 biol ×2 NTC H3K27Ac biol ×2 NTC. H3K79me2 biol ×2 NTC Input biol ×2 shMed4 #1 H3K4me1 biol ×2 shMed4 #1 H3K4me3 biol ×2 +10 more

Supports a between-group comparison across 36 samples.

How we read this: 18 replicated groups read from 36 sample titles; they account for 36 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
Datasets on a similar topic

Search all mouse ChIP / ATAC / CUT&Tag 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.