GEO series

Estrogen receptor β target gene expression reveals novel repressive functions in aggressive breast cancer [ChIP-Seq]

GSE274448 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 24 samples Submitted 2026/02/15 Platform GPL18573

At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 24 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)
Topic: Breast cancerThis series is part of our curated briefing on it.
Samples: 24 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: Estrogen receptor β target gene expression reveals novel repressive functions in aggressive breast cancerNPJ breast cancer · 2026

Summary (written by the submitters)

Inflammatory breast cancer (IBC) is a highly metastatic breast carcinoma with high frequency of estrogen receptor a (ERα) negativity and limited treatment options. We previously explored the second ER subtype, (ERβ) and reported correlation of its tumor expression with reduced metastasis in patients and in preclinical models of the disease.

Read the full summary ↓

We initially associated the anti-metastatic function of the receptor with the inhibition of actin-based cell migration and the associated Rho GTPase signaling in IBC cells. We have now followed an integrated genomics approach to fully delineate the signaling underlying the anti-metastatic effects of ERβ. Through mapping binding sites in IBC cells that express endogenous and transfected ERβ in the presence of an agonist and interrogating this information with altered expression of protein coding mRNAs and miRNAs we have defined the interaction of a biologically active receptor with the cancer genome that controls metastatic signals. We reveal key regulatory chromatin binding sites and motifs and identify direct target genes and miRNAs and the associated biological functions. Our new findings implicate the regulation of metabolic pathways and signaling in development and tumor microenvironment in anti-metastatic activity of ERβ. Through a rigorous analysis of target genes in clinical datasets we also associate downstream factors with patient outcomes reporting new molecules with targeting potential and strengthening the relevance of ERβ signaling for the metastatic process in breast cancer. Our findings thus offer an opportunity to validate the tumor repressive role of ERβ through a better understanding of its mechanism of action.

Published in

Estrogen receptor β target gene expression reveals novel repressive functions in aggressive breast cancer

Tastsoglou S, Karagounis IV, Miliotis M et al. · NPJ breast cancer 2026 · PMID 41654535 · doi:10.1038/s41523-026-00905-4

This dataset

Open GSE274448 in finder → Find more human ChIP / ATAC / CUT&Tag datasets → Breast cancer 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 GSE274448_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 PRJNA1146439 and SRA study SRP525473. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 41654535) ↗

Samples in this study

The sample list for this study is not cached yet. Press Load samples and it will be fetched from NCBI.

+ 24 more — browse all 24 samples with per-sample file links →

More Breast cancer datasets

GSE10886 A Supervised Risk Predictor of Breast Cancer Based on Biological Subtypes 226 samples same disease briefing · shares breast
GSE11121 The humoral immune system has a key prognostic impact in node-negative breast cancer 200 samples same disease briefing · shares breast
GSE104193 Hypoxia-mediated translational activation of ITGB3 in breast cancer cells enhances TGF-β signalling and malignant features in vitro and in vivo 32 samples same disease briefing · shares breast
GSE104675 Role for the Transcriptional Activator ZRF1 in Breast Cancer Progression and Endocrine Resistance 6 samples same disease briefing · shares breast
GSE10885 An integromic analysis reveals that metaplastic carcinomas are distinct from basal-like tumors. 244 samples same disease briefing
GSE298767 Dose-dependent Effects of Estrogen on Genomic Regulation in Breast Cancer Cells [ChIP-seq] 63 samples shares estrogen, chip-seq, breast
GSE301553 The impact of Fulvestrant on Estrogen Receptor-Driven Chromatin Dynamics in breast cancer cells points to a disconnect between chromatin opening and histone acetylation [CUT&Tag] 18 samples shares estrogen, receptor, breast
GSE284956 Overcoming intrinsic mechanisms of cell cycle inhibitor resistance in estrogen receptor-positive (ER+) breast cancer 180 samples shares estrogen, receptor, breast

Search all human 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.