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UBR7 in concert with EZH2 inhibits the TGF-β signalling leading to extracellular matrix remodelling [ChIP-seq]

GSE262487 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 14 samples Submitted 2025/03/26 Platform GPL24676
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 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
Homo sapiens (human)
Topic
Breast cancerThis series is part of our curated briefing on it.
Samples
14 samples: 7 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.
Summary (written by the submitters)
The intricate interplay between resident cells and the extracellular matrix (ECM) wields a profound influence on cancer progression. In Triple Negative Breast Cancer (TNBC), ECM architecture evolves primarily due to the enrichment of lysyl oxidase, fibronectin, and collagen that eventually promote distant metastasis. Here, we have uncovered a pivotal transcription regulatory mechanism of the epigenetic regulator UBR7 in conjunction with histone methyltransferase EZH2 in regulating TGF-b/Smad signalling-axis thereby fine-tuning the ECM genes.
Read the full summary ↓
Remarkably, UBR7 loss leads to a dramatic reduction in the facultative heterochromatin mark H3K27me3 in chromatin, leading to ECM genes firing. Apart from playing a seminal role in matrix deposition in adherent-cancer cells and spheroids, UBR7 alters the total collagen content and lysyl oxidase activity thereby directly impacting the matrix stiffness and consequently its invasive properties. These results can be further translated to TNBC-patients, where reduced RNA/protein levels of UBR7 is accompanied by heightened expression of the ECM-components and their functional-activity which is responsible for fibrosis-mediated matrix stiffness. Thus, UBR7 acts as a master regulator of TNBC matrix-stiffening thereby impacting its metastatic potential.
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 GSE262487_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 PRJNA1107816 and SRA study SRP506827. Searching any of these in the dataset finder brings you back here.

Study design
7 conditions, mostly in duplicate
Scrambled Input / Whole Cell Extract DNA ×2 UBR7 silenced cells Input / Whole Cell Extrac… ×2 Chromatin Immunoprecipitate of H3k27Ac from W… ×2 Chromatin Immunoprecipitate of H3k27Me3 from … ×2 Chromatin Immunoprecipitate of H3k27Ac from U… ×2 Chromatin Immunoprecipitate of H3k27Me3 from … ×2 Chromatin Immunoprecipitate of UBR7 from Wild… ×2

Supports a case/control comparison: 4 samples read as cases, 8 as controls.

How we read this: 7 replicated groups read from 14 sample titles; they account for 14 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
More Breast cancer datasets

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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.