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Fibroblast STAT3 activation drives organ-specific premetastatic niche formation

GSE292712 Mus musculus (mouse) RNA-seq (gene expression) 27 samples Submitted 2025/10/07 Platform GPL24247
At a glance

RNA-seq (gene expression) · mouse · 27 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
27 samples: 8 conditions, mostly in triplicateGroups 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
Fibroblast STAT3 Activation Drives Organ-Specific Premetastatic Niche FormationCancer research · 2026
Summary (written by the submitters)
Pancreatic cancer is associated with a high rate of metastasis and poor prognosis. The formation of a premetastatic niche (PMN) facilitates cancer cell spread and contributes to cancer mortality. Using murine pancreatic cancer models based on expression of oncogenic KRAS in the pancreas epithelium, we discovered that remodeling of the lung microenvironment occurred in mice bearing pancreatic precursor lesions prior to cancer formation.
Read the full summary ↓
This early lesion premetastatic niche (EL-PMN) resembled the PMN in cancer-bearing mice, and both feature characteristics of overt metastasis, such as transcriptional reprogramming, activation of fibroblast STAT3 signaling, and infiltration of immunosuppressive ARG1+ macrophages. Both pancreatic cancer patients and mouse models demonstrated elevated serum IL6. Inactivating oncogenic KRAS reduced serum IL6 and reverted fibroblast STAT3 phosphorylation in mouse lungs; loss of lung fibroblast STAT3 phosphorylation was similarly observed when mice were treated with the pan-RAS inhibitor RMC7977. While ARG1+ macrophage infiltration was dispensable for fibroblast STAT3 activation, IL6 blockade inhibited lung fibroblast STAT3 activation. Functionally, fibroblast STAT3 activation was necessary for lung metastasis establishment and growth. Interestingly, activation of STAT3 in the PMN was present in the lungs but not in the liver, where fibroblast reprogramming occurred only in overt metastasis, pointing to organ-specific PMN formation. In human metastasis samples, phosphorylated STAT3 in fibroblasts was similarly more abundant in the lungs than liver. Together, these data point to organ-specific mechanisms driving formation of the PMN and indicate that reprogramming of the microenvironment prior to metastasis might support early dissemination of pancreatic cancer.
Published in
Fibroblast STAT3 Activation Drives Organ-Specific Premetastatic Niche Formation
Lasse Opsahl EL, Espinoza CE, Olivei AC et al. · Cancer research 2026 · PMID 41105672 · doi:10.1158/0008-5472.CAN-25-3472
This dataset
Open GSE292712 in finder → Find more mouse RNA-seq 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 GSE292712_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: 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 PRJNA1241135 and SRA study SRP572811. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 41105672) ↗
Study design
8 conditions, mostly in triplicate
iKRAS, 16 weeks ON dox - lung ×3 Control, 16 weeks ON dox - lung ×3 Control, 16 weeks ON dox - pancreas ×3 iKRAS, 16 weeks ON - pancreas ×3 Control, 20 weeks ON dox - lung ×2 iKRAS, 16 weeks ON + 1 week OFF - lung ×2 iKRAS, 16 weeks ON + 1 week OFF - pancreas ×2 Control, 20 weeks ON dox - pancreas ×2 +7 more

Supports a case/control comparison: 2 samples read as cases, 12 as controls.

How we read this: 8 replicated groups read from 27 sample titles; they account for 20 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
Datasets on a similar topic

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