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Cancer cells subvert ZNF93 to escape surveillance by L1 epigenetic sentinels and control APOBEC3B [cutandtag]

GSE290773 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 14 samples Submitted 2025/08/01 Platform GPL18573
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)
Samples
14 samples: 4 × H3K4_sc vs 4 × H3K4_93v vs 3 × H3K9_sc vs 3 × H3K9_93vGroups 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
Cancer cells subvert the primate-specific KRAB zinc finger protein ZNF93 to control APOBEC3BProceedings of the National Academy of Sciences of the United States of America · 2025
Summary (written by the submitters)
The primate-restricted KRAB zinc finger protein (KZFP) ZNF93 represses a subset of L1 transposable elements (TEs) that propagated in the human ancestral genome some 20 to 12 million years ago and have all become transposition-incompetent due to inactivating mutations. Here, we demonstrate that these L1 integrants encode a highly genotoxic endonuclease, and that ZNF93 also represses other full-length L1 integrants via indirect effects as well as APOBEC3B.
Read the full summary ↓
Consistent with the exquisite sensitivity of single-stranded DNA to attack by both the L1 endonuclease and the cytidine deaminase, ZNF93 expression peaks in S phase and correlates with cell proliferation. ZNF93 is induced in most cancers, and ZNF93-depleted cells exhibit defects in DNA synthesis and activation of the replication and DNA damage checkpoints. These results suggest a model whereby ZNF93 is a major guardian of genome integrity subverted by cancer cells to escape L1-mediated epigenetic surveillance and achieve a proper balance of APOBEC3B-induced tumor heterogeneity and overall genome stability.
Published in
Cancer cells subvert the primate-specific KRAB zinc finger protein ZNF93 to control APOBEC3B
Forey R, Raclot C, Pulver C et al. · Proceedings of the National Academy of Sciences of the United States of America 2025 · PMID 40828019 · doi:10.1073/pnas.2505021122
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 GSE290773_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 PRJNA1230089 and SRA study SRP567197. Searching any of these in the dataset finder brings you back here.

Study design
4 × H3K4_sc vs 4 × H3K4_93v vs 3 × H3K9_sc vs 3 × H3K9_93v

Supports a between-group comparison across 14 samples.

How we read this: 4 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
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