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NCOR2 represses MHC class I molecule expression to drive metastatic progression of breast cancer

GSE320158 Mus musculus (mouse) ChIP-seq / ATAC-seq (genome binding and open chromatin) 14 samples Submitted 2026/07/15 Platform GPL34328
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · mouse · 14 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
14 samples
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
NCOR2 represses MHC class I molecule expression to drive metastatic progression of breast cancerNature communications · 2026
Summary (written by the submitters)
Metastatic progression depends upon the ability of disseminated tumor cells to evade immune surveillance. MHC-mediated antigen presentation facilitates T cell-dependent eradication of metastatic tumor cells. We identified nuclear corepressor 2 (NCOR2) as an epigenetic regulator of MHC class I molecule presentation on breast tumor cells.
Read the full summary ↓
Patients with triple negative breast cancers (TNBC) that expressed high levels of NCOR2 also exhibited reduced metastasis-free survival and decreased MHC class I expression, and metastatic lesions in patients with TNBC had high nuclear NCOR2 and reduced CD8+ T cells. Reducing NCOR2 expression or preventing its interaction with HDAC3 enhanced innate immune cell recruitment and activity, and elevated MHC class I levels on disseminated cancer cells to potentiate CD8+ T cell activity and apoptosis induction that prevented metastatic progression. The studies provide evidence to support NCOR2 as a targetable epigenetic regulator of metastasis towards which therapies could be developed to reduce patient mortality.
Published in
NCOR2 represses MHC class I molecule expression to drive metastatic progression of breast cancer
Ticha P, Northey JJ, Narain R et al. · Nature communications 2026 · PMID 42086546 · doi:10.1038/s41467-026-72168-3
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 GSE320158_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 PRJNA1426978 and SRA study SRP678682. Searching any of these in the dataset finder brings you back here.

Samples in this study

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+ 14 more — browse all 14 samples with per-sample file links →

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