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Loss of ARID1A leads to a cold tumor phenotype via suppression of IFNγ signaling

GSE277050 Homo sapiens (human) RNA-seq (gene expression) 12 samples Submitted 2025/01/01 Platform GPL21290
At a glance

RNA-seq (gene expression) · human · 12 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
12 samples: 3 × SK-N-DZ Control vs 3 × SK-N-DZ Dox vs 3 × SK-N-DZ IFN vs 3 × SK-N-DZ Dox IFNGroups 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
Loss of ARID1A leads to a cold tumor phenotype via suppression of IFNγ signalingScientific reports · 2025
Summary (written by the submitters)
The collapse of inflammatory signaling that recruits cytotoxic immune cells to the tumor microenvironment contributes to the immunologically cold tumor phenotype in neuroblastoma (NB) and is a barrier to NB immunotherapy. Multiple studies have reported that MYCN amplification, a trait of high-risk NB, correlates with a loss of inflammatory signaling; but MYCN also correlates with 1p36 deletions in NB where the SWI/SNF chromatin remodeling complex subunit ARID1A (1p36.11) is located.
Read the full summary ↓
ARID1A is known to support inflammatory signaling in adult cancers but its role in NB inflammatory signaling is unexplored. We find MYCN overexpression causes a stronger and ARID1A knockdown causes a weaker inflammatory response to interferon-gamma (IFNγ). ARID1A silencing reduces IFNγ induced gene signatures for the transcription factor interferon response factor 1 (IRF1). We found ARID1A is a functional interactor of IRF1 by co-immunoprecipitation studies, and ARID1A silencing causes loss of activating chromatin marks at the IRF1 target gene CXCL10. We model that IRF1 uses ARID1A containing SWI/SNF to promote IRF1’s target genes in response to IFNγ. This work finds that ARID1A is a critical regulator of inflammatory signaling in NB and provides rationale for testing immune therapies in MYCN amplified NB that are effective in adult ARID1A mutated cancers.
Published in
Loss of ARID1A leads to a cold tumor phenotype via suppression of IFNγ signaling
Watson PM, DeVaux CA, Freeman KW · Scientific reports 2025 · PMID 40082458 · doi:10.1038/s41598-025-91688-4
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 GSE277050_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 PRJNA1160289 and SRA study SRP532349. Searching any of these in the dataset finder brings you back here.

Study design
3 × SK-N-DZ Control vs 3 × SK-N-DZ Dox vs 3 × SK-N-DZ IFN vs 3 × SK-N-DZ Dox IFN

Supports a between-group comparison across 12 samples.

How we read this: 4 replicated groups read from 12 sample titles; they account for 12 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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