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The interleukin 22–oncostatin M axis promotes intestinal inflammation and tumorigenesis [Colon_Tissue_BulkRNA-seq]

GSE269506 Mus musculus (mouse) RNA-seq (gene expression) 22 samples Submitted 2025/03/27 Platform GPL24247
At a glance

RNA-seq (gene expression) · mouse · 22 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
Mus musculus (mouse)
Samples
22 samples: 5 × Col_Col1a2, colitis, day21, E1_1 vs 4 × Col_Cadh5, colitis, day 21, E2_1 vs 3 × Col_Villin, colitis, day 21, E2_1 vs 2 × Col_Villin, colitis, day 21, E1_1Groups 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
The IL-22-oncostatin M axis promotes intestinal inflammation and tumorigenesisNature immunology · 2025
Summary (written by the submitters)
Multicellular cytokine networks regulate the onset of intestinal inflammation and colitis-associated cancer (CAC). Interleukin 22 (IL-22) promotes epithelial cell recovery but can also drive inflammation and tumorigenesis. We demonstrate that IL-22 from innate lymphoid cells activates STAT3 and increases OSM receptor expression in intestinal epithelial cells.
Read the full summary ↓
This activation leads to sustained STAT3 activity via OSM, promoting inflammation and tumorigenesis. Deleting the OSM receptor or blocking OSM pharmacologically mitigates colitis and CAC. Our findings highlight the IL-22-OSM axis as a potential therapeutic target for these conditions.
Published in
The IL-22-oncostatin M axis promotes intestinal inflammation and tumorigenesis
Cineus R, Luo Y, Saliutina M et al. · Nature immunology 2025 · PMID 40447860 · doi:10.1038/s41590-025-02149-z
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 GSE269506_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 PRJNA1122159 and SRA study SRP512985. Searching any of these in the dataset finder brings you back here.

Study design
5 × Col_Col1a2, colitis, day21, E1_1 vs 4 × Col_Cadh5, colitis, day 21, E2_1 vs 3 × Col_Villin, colitis, day 21, E2_1 vs 2 × Col_Villin, colitis, day 21, E1_1

Supports a between-group comparison across 14 samples.

How we read this: 4 replicated groups read from 22 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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