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The extracellular matrix drives guanylate production and protects pancreatic cancer cells from oxaliplatin-induced DNA damage.

GSE284085 Mus musculus (mouse) RNA-seq (gene expression) 12 samples Submitted 2025/11/13 Platform GPL24247

At a glance

RNA-seq (gene expression) · mouse · 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: Mus musculus (mouse)
Samples: 12 samples: 3 × Primary Tumor 1, ECM substrate, Normoxia, vs 3 × Primary Tumor 1, No substrate, Normoxia, vs 3 × Primary Tumor 2, ECM substrate, Normoxia, vs 3 × Primary Tumor 2, No substrate, Normoxia,Groups 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 extracellular matrix drives guanylate production and protects pancreatic cancer cells from oxaliplatin-induced DNA damageScience advances · 2025

Summary (written by the submitters)

The excessive production of extracellular matrix (ECM) and the metabolic adaptations in pancreatic ductal adenocarcinoma (PDAC) contribute individually to enhanced chemoresistance, dramatic tumor progression and dismal patient survival. However, the ECM-driven metabolic alterations that promote chemoresistance in PDAC are less well described.

Read the full summary ↓

Here, we use in-vitro-generated ECM bio-scaffolds that recapitulate cell-ECM interactions and induce broad metabolic alterations in PDAC cells. High-throughput integration of multi-omics datasets coupled with metabolic tracing showed that the ECM favors the accumulation of guanylates in PDAC cells and alleviation of oxaliplatin-induced DNA damage, thus supporting PDAC cell proliferation. This is controlled by the GMP-producing enzyme IMPDH, the expression of which was upregulated in resected PDAC tissue from patients who displayed low survival. We propose that targeting ECM-modulated metabolic processes in PDAC may be a more effective and safer approach, without the negative side effects of direct targeting of the ECM itself.

Published in

The extracellular matrix drives guanylate production and protects pancreatic cancer cells from oxaliplatin-induced DNA damage

Efthymiou G, Lohmann E, Montenegro C et al. · Science advances 2025 · PMID 41385622 · doi:10.1126/sciadv.adu2276

This dataset

Open GSE284085 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 GSE284085_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 PRJNA1196972 and SRA study SRP550916. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 41385622) ↗

Study design

3 × Primary Tumor 1, ECM substrate, Normoxia, vs 3 × Primary Tumor 1, No substrate, Normoxia, vs 3 × Primary Tumor 2, ECM substrate, Normoxia, vs 3 × Primary Tumor 2, No substrate, Normoxia,

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

GSM8677757 Primary Tumor 1, ECM substrate, Normoxia, Replicate 1 Primary Tumor 1, ECM su…
GSM8677758 Primary Tumor 1, ECM substrate, Normoxia, Replicate 2 Primary Tumor 1, ECM su…
GSM8677759 Primary Tumor 1, ECM substrate, Normoxia, Replicate 3 Primary Tumor 1, ECM su…
GSM8677760 Primary Tumor 1, No substrate, Normoxia, Replicate 1 Primary Tumor 1, No sub…
GSM8677761 Primary Tumor 1, No substrate, Normoxia, Replicate 2 Primary Tumor 1, No sub…
GSM8677762 Primary Tumor 1, No substrate, Normoxia, Replicate 3 Primary Tumor 1, No sub…
GSM8677763 Primary Tumor 2, ECM substrate, Normoxia, Replicate 1 Primary Tumor 2, ECM su…
GSM8677764 Primary Tumor 2, ECM substrate, Normoxia, Replicate 2 Primary Tumor 2, ECM su…
GSM8677765 Primary Tumor 2, ECM substrate, Normoxia, Replicate 3 Primary Tumor 2, ECM su…
GSM8677766 Primary Tumor 2, No substrate, Normoxia, Replicate 1 Primary Tumor 2, No sub…
GSM8677767 Primary Tumor 2, No substrate, Normoxia, Replicate 2 Primary Tumor 2, No sub…
GSM8677768 Primary Tumor 2, No substrate, Normoxia, Replicate 3 Primary Tumor 2, No sub…

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