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ARID1A recruits non-homologous end joining factors to DNA breaks induced by G4 ligands

GSE295547 Homo sapiens (human) RNA-seq (gene expression) 14 samples Submitted 2025/08/13 Platform GPL24676
At a glance

RNA-seq (gene expression) · human · 14 samples

What it is
RNA-seq (gene expression)Gene activity measured by sequencing. The summary does not mention single-cell work, so this is most likely bulk: one average per sample, the usual starting point for comparing groups.
Organism
Homo sapiens (human)
Samples
14 samples: 6 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.
Paper
ARID1A stabilizes non-homologous end joining factors at DNA breaks induced by the G4 ligand pyridostatinCell reports · 2025
Summary (written by the submitters)
ARID1A, a subunit of the BAF chromatin remodeler, is frequently mutated in cancer. Predicting how ARID1A loss impacts cancer therapy response is challenging because it influences many cellular pathways. G quadruplex (G4) binding ligands, such as pyridostatin, show anticancer effects, but the genetic determinants influencing the response to G4 ligands are not fully understood.
Read the full summary ↓
Here, we show that ARID1A-deficient cells are selectively sensitive to pyridostatin compared to isogenic controls. This was apparent in ovarian and colorectal cancer cell line models, and in vivo studies suggest that G4 ligands hold promise for ARID1A-deficient cancers. While ARID1A modulates pyridostatin-induced transcriptional responses, we show that toxicity in ARID1A-deficient cells arises from the defective repair of topoisomerase-induced breaks. Notably, these cells fail to efficiently accumulate non-homologous end joining proteins on chromatin following pyridostatin exposure. These data uncover a role for ARID1A in the cellular response to G4 ligands, linking remodeling to G4 ligand-induced responses.
Published in
ARID1A stabilizes non-homologous end joining factors at DNA breaks induced by the G4 ligand pyridostatin
Simões-Sousa S, Amin N, Lane KA et al. · Cell reports 2025 · PMID 40938753 · doi:10.1016/j.celrep.2025.116277
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 GSE295547_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: For RNA-seq the counts are usually a table among the supplementary files (look for 'counts', 'expression', 'FPKM' or 'TPM' in the file name). The series matrix of a sequencing study is sometimes nearly empty.

Also filed as BioProject PRJNA1255162 and SRA study SRP581153. Searching any of these in the dataset finder brings you back here.

Study design
6 conditions, mostly in duplicate
TOV21G parental, PDS-treated, ×3 TOV21G parental, untreated, ×3 TOV21G +ARID1A, clone 1 (TOV8), PDS-treated, ×2 TOV21G + ARID1A, clone 1 (TOV8), untreated, ×2 TOV21G + ARID1A, clone 2 (TOV18), PDS-treated, ×2 TOV21G + ARID1A, clone 2 (TOV18), untreated, ×2

Supports a between-group comparison across 14 samples.

How we read this: 6 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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