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

GSE271301 Homo sapiens (human) RNA-seq (gene expression) 28 samples Submitted 2025/03/04 Platform GPL24676
At a glance

RNA-seq (gene expression) · human · 28 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
28 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
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
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 GSE271301_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 PRJNA1130888 and SRA study SRP517509. Searching any of these in the dataset finder brings you back here.

Samples in this study

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