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Replication stress underlies genomic instability at CTCF/cohesin-binding sites in cancer

GSE292153 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 32 samples Submitted 2025/03/22 Platform GPL16791Platform GPL24676
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 32 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)
Samples
32 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
CTCF/cohesin-binding sites are susceptible to replication-associated DNA damage and genomic instability in cancer cellsiScience · 2026
Summary (written by the submitters)
CCCTC-binding factor (CTCF) and cohesin play a significant role in the formation of chromatin loops and topologically associating domains (TADs), which influence gene expression and DNA replication. CTCF/cohesin-binding sites (CBSs) present at the loop anchors and TAD boundaries are frequently mutated in cancer; however, the molecular mechanisms underlying this remain unclear.
Read the full summary ↓
Here, we investigate whether the binding of CTCF/cohesin on DNA imposes constraints on DNA replication, leading to replication stress and genomic instability. Our results reveal that CTCF and cohesin remain cobound to DNA during replication (S phase) in cancer cells (HeLa). Further, examination of replication stress through ChIP-seq of the DNA damage response/repair proteins (MRE11, STN1, FANCD2, γH2AX, RAD51 and ATM) showed high enrichment of these proteins at CBSs (as compared to their immediate flanking regions and control sites) and positively correlated with the binding strength of CTCF/cohesin at CBSs in the S phase. Moreover, analysis of somatic mutations from cancer genomes supports that the enrichment of mutations at CBSs is significantly higher in samples harbouring somatic copy number deletion in MRE11 and STN1 compared to wild-type samples. Together, these results demonstrate that the co-binding of CTCF/cohesin on the DNA during the S phase causes replication stress and DNA strand breaks, and this could lead to genome instability at CBSs observed in cancer.
Published in
CTCF/cohesin-binding sites are susceptible to replication-associated DNA damage and genomic instability in cancer cells
Faseela EE, Notani D, Sabarinathan R · iScience 2026 · PMID 41630911 · doi:10.1016/j.isci.2026.114646
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 GSE292153_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 PRJNA1237290 and SRA study SRP571899. Searching any of these in the dataset finder brings you back here.

Samples in this study

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