GEO series

Multidimensional OMICs reveal ARID1A orchestrated control of DNA damage, splicing, and cell cycle in normal and malignant urothelial cells [ATAC-seq]

GSE271587 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 10 samples Submitted 2025/03/04 Platform GPL24676

At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 10 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: 10 samples: 5 × UROtsa, NTC vs 4 × UROtsa, ARID1A gRNA3Groups 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: Multidimensional OMICs reveal ARID1A orchestrated control of DNA damage, splicing, and cell cycle in normal-like and malignant urothelial cellsMolecular oncology · 2025

Summary (written by the submitters)

Epigenetic regulators, such as the SWI/SNF complex, play an important role in tissue development and homeostasis, and are frequently mutated in cancer. ARID1A, a subunit of the SWI/SNF complex, is mutated in approximately 20% of all bladder tumors, however, our understanding of the consequences thereof remains limited. Here, we generated various loss- and gain-of-function models to conduct Omni-ATAC-Seq, RNA-Seq, interactome analyses, and first functional studies to characterize ARID1A-affected pathways potentially suitable for the treatment of ARID1A-deficient bladder cancers.

Read the full summary ↓

We observed decreased cell proliferation and deregulation of stress-regulated pathways including DNA repair in ARID1A-deficient cells. Furthermore, ARID1A was linked to alternative splicing and translational regulation on RNA and interactome levels. The absence of ARID1A drastically impacted the accessibility of chromatin, displaying significantly less accessible chromatin especially around distal, but not proximal, enhancers. Less accessible chromatin areas were mapped to pathways such as DNA damage response and cell proliferation. Indeed, the G2/M checkpoint appeared impaired after DNA damage in ARID1A-deficient cells. Together, this highlights the broad impact of ARID1A and the possibility of targeting proliferative and DNA repair pathways.

Published in

Multidimensional OMICs reveal ARID1A orchestrated control of DNA damage, splicing, and cell cycle in normal-like and malignant urothelial cells

Schlösser RM, Krumbach F, Corrales E et al. · Molecular oncology 2025 · PMID 40170512 · doi:10.1002/1878-0261.70019

This dataset

Open GSE271587 in finder → Find more human ChIP / ATAC / CUT&Tag datasets →

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 GSE271587_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 PRJNA1132254 and SRA study SRP518207. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 40170512) ↗

Study design

5 × UROtsa, NTC vs 4 × UROtsa, ARID1A gRNA3

Supports a between-group comparison across 9 samples.

How we read this: 2 replicated groups read from 10 sample titles; they account for 9 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

GSM8380152 UROtsa, NTC1 UROtsa, NTC
GSM8380153 UROtsa, NTC4 UROtsa, NTC
GSM8380154 UROtsa, NTC6 UROtsa, NTC
GSM8380155 UROtsa, NTC8 UROtsa, NTC
GSM8380156 UROtsa, NTC10 UROtsa, NTC
GSM8380157 UROtsa, ARID1A gRNA3 5 UROtsa, ARID1A gRNA3
GSM8380158 UROtsa, ARID1A gRNA3 13 UROtsa, ARID1A gRNA3
GSM8380159 UROtsa, ARID1A gRNA2 14
GSM8380160 UROtsa, ARID1A gRNA3 29 UROtsa, ARID1A gRNA3
GSM8380161 UROtsa, ARID1A gRNA3 31 UROtsa, ARID1A gRNA3

Datasets on a similar topic

GSE271687 Multidimensional OMICs reveal ARID1A orchestrated control of DNA damage, splicing, and cell cycle in normal and malignant urothelial cells 38 samples shares arid1a, multidimensional, orchestrated, urothelial, malignant, splicing, control
GSE271301 Multidimensional OMICs reveal ARID1A orchestrated control of DNA damage, splicing, and cell cycle in normal and malignant urothelial cells [RNA-seq] 28 samples shares arid1a, multidimensional, orchestrated, urothelial, malignant, splicing, control
GSE249439 ARID1A regulates DSB repair through chromatin organization and its deficiency triggers DNA damage-mediated immune response [ATAC-seq] 48 samples shares arid1a, atac-seq
GSE253703 IRF4 requires ARID1A to establish plasma cell identity in multiple myeloma (ATAC-Seq human 16) 16 samples shares arid1a, atac-seq
GSE253706 IRF4 requires ARID1A to establish plasma cell identity in multiple myeloma (ATAC-Seq human 8) 8 samples shares arid1a, atac-seq
GSE254864 Deciphering the novel regulatory mechanisms and biological implications of ARID1A C-terminal missense mutations in cancer [ATAC-Seq] 6 samples shares arid1a, atac-seq
GSE176493 Comprehensive target engagement by EZH2 inhibitor CPI-0209 allows for preferential targeting of ARID1A mutant urothelial carcinoma 252 samples shares arid1a, urothelial
GSE176477 Epigenomic change of ARDI1A mutant bladder cancer cell line treated with CPI-0209 or induced ARID1A expression 48 samples shares arid1a

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