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A conserved epithelial wound-like transcriptional program driven by FOSL1 underlies malignant progression of pancreatic ductal adenocarcinoma (ssRNA-Seq)

GSE248585 Mus musculus (mouse) RNA-seq (gene expression) 46 samples Submitted 2026/04/30 Platform GPL24247
At a glance

RNA-seq (gene expression) · mouse · 46 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
46 samples: 16 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.
Summary (written by the submitters)
Pancreatic ductal adenocarcinoma (PDAC) is the deadliest common malignancy1. Benign lesions named pancreatic intraepithelial neoplasia (PanIN) are important precursors to PDAC, but these are extremely common in the general population2. The mechanisms underlying the lethal conversion of benign PanINs to invasive PDAC is poorly understood.
Read the full summary ↓
Here we harness Stereo-seq, a high resolution spatial transcriptomic profiling platform3, to identify a core transcriptional program associated with invasive growth in human PDAC. This program, highly conserved in mice, is primarily comprised of genes activated to drive the migration of keratinocytes during wound healing in the skin. Genes of this wound-like program are required for conversion of PanINs into invasive PDAC in mice. Benign PanINs continually produce a small reservoir of wound-like cells that activate key tumor suppressor genes (TSGs), keeping the incipient malignant cells in check. TSG KO in PanIN leads to rapid outgrowth of the wound-like population, unleashing invasive growth. Wound-induced AP-1 transcription factors (TFs) FOSL1 and JUNB are specifically activated in invasive PDAC cells and enforced expression of FOSL1 in PanIN drives wound-like gene expression and benign-to-malignant plasticity. Malignant PDAC cells are surrounded by a conserved population of CTHRC1-expressing cancer-associated fibroblasts (CAFs) that possess a transcriptional program strikingly similar to one activated in a population of wound-emergent fibroblasts in skin. Bidirectional interactions between malignant cancer cells and the wound-like CAFs result in a feedback loop that enforces the malignant state.
This dataset
Open GSE248585 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 GSE248585_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 PRJNA1044815 and SRA study SRP474053. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗
Study design
16 conditions, mostly in triplicate
Pdx1_KrasG12D, PanIN, Biological replicate1-T… ×3 Pdx1_KrasG12D, PanIN, Biological replicate2-T… ×3 Pdx1_KrasG12D, PanIN, Biological replicate3-T… ×3 Pdx1_KrasG12D_Trp53fl/fl, PDAC, Biological re… ×3 Ptf1a-CreERT2_KrasG12D, OE tBFP, Biological r… ×3 Ptf1a-CreERT2_KrasG12D, OE tBFP, Biological r… ×3 Ptf1a-CreERT2_KrasG12D, OE FOSL1_tBFP, Biolog… ×3 Ptf1a-CreERT2_KrasG12D, OE FOSL1_tBFP, Biolog… ×3 +8 more

Supports a between-group comparison across 46 samples.

How we read this: 16 replicated groups read from 46 sample titles; they account for 46 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

+ 6 more — browse all 46 samples with per-sample file links →

Datasets on a similar topic

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