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A hyperactive splice variant of STAT3 promotes colonic inflammation-associated tumorigenesis in mice

GSE270970 Mus musculus (mouse) RNA-seq (gene expression) 10 samples Submitted 2025/12/10 Platform GPL34328
At a glance

RNA-seq (gene expression) · mouse · 10 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
10 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
A hyperactive splice variant of STAT3 promotes colonic inflammation-associated tumorigenesis in miceScience translational medicine · 2025
Summary (written by the submitters)
Signal transducer and activator of transcription 3 (STAT3) is essential for cell signaling in response to extracellular stimuli, and its overactivation is a hallmark of inflammation and tumorigenesis. The differential mechanisms underlying the physiological and pathological regulation of STAT3 remain elusive. Here we demonstrate that cryptic splice sites in STAT3 generate heterogeneous isoforms with or without a single amino acid S701 (wS701/ΔS701), with the latter being substantially upregulated in colon cancers.
Read the full summary ↓
Intrinsic S701 undergoes reversible phosphorylation catalyzed by mTOR complex 1 (mTORC1) and protein phosphatase 2A (PP2A). Upon inflammatory stimulation, precursor phosphorylation at S701 sequesters Y705 phosphorylation by interfering with the access of janus kinase 1/2 (JAK1/2), and restricts STAT3 overactivation. In contrast, the ΔS701 isoform is hyperactive due to absence of this self-restricting mechanism. Deletion of S701 in mice increases susceptibility to colonic inflammation and tumorigenesis. Pharmacological inhibition of PP2A sustains S701 phosphorylation, and alleviates colon inflammation in wild-type but not in ΔS701 mice. Our findings highlight the importance of STAT3 heterogeneity in human diseases.
Published in
A hyperactive splice variant of STAT3 promotes colonic inflammation-associated tumorigenesis in mice
Xu M, Wei D, Zhong S et al. · Science translational medicine 2025 · PMID 41370399 · doi:10.1126/scitranslmed.adu8484
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 GSE270970_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 PRJNA1129127 and SRA study SRP516634. Searching any of these in the dataset finder brings you back here.

Samples in this study

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