GEO series

Antithrombin-binding heparan sulfate is ubiquitously expressed in epithelial cells and suppresses pancreatic tumorigenesis

GSE270542 Mus musculus (mouse) RNA-seq (gene expression) 18 samples Submitted 2025/08/05 Platform GPL24247

At a glance

RNA-seq (gene expression) · mouse · 18 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: 18 samples: 10 × Tumor, HS3ST1 KO, vs 8 × Tumor, WT,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: Antithrombin-binding heparan sulfate is ubiquitously expressed in epithelial cells and suppresses pancreatic tumorigenesisThe Journal of clinical investigation · 2025

Summary (written by the submitters)

3-O-sulfation of heparan sulfate is the key determinant for the binding and activation of the serine protease inhibitor antithrombin. This interaction is the basis of the anti-thrombotic treatment using heparin, a fractionated form of heparan sulfate derived from porcine entrails and bovine lung. Antithrombin-binding heparan sulfate (HSAT) is also expressed in human tissues, although it is generally thought to be rare and restricted to endothelial cells, mast cells, or follicular fluid.

Read the full summary ↓

Here we show that HSAT is ubiquitously expressed in the basement membranes of epithelial cells in multiple tissues, indicating that HSAT is more abundant than previously realized. HSAT is expressed by healthy pancreatic ductal cells and its expression is increased in neoplastic progression of premalignant pancreatic intraepithelial neoplasia lesions (PanINs) but reduced in mature metastatic pancreatic ductal adenocarcinoma (PDAC). Genetic inactivation of HS3ST1, a key enzyme in HSAT synthesis, in murine PDAC cells eliminated HSAT expression, induced an inflammatory phenotype, suppressed markers of apoptosis, and increased metastasis in an experimental mouse model. HSAT-positive PDAC tumors bind AT, which inhibits the generation of active thrombin by tissue factor (TF) and Factor VIIa. These findings suggest that expression of HSAT acts as a tumor suppressor through recruitment of AT and that the loss of HSAT in progression to PDAC increases inflammation and metastatic potential. Furthermore, plasma from PDAC patients showed an accumulation of HSAT suggesting its possible utility as a marker of tumor formation. Fully understanding the function of HSAT in healthy tissues and how it contributes to pancreatic tumorigenesis could pave the way for the development of novel strategies for early diagnosis and potential therapy.

Published in

Antithrombin-binding heparan sulfate is ubiquitously expressed in epithelial cells and suppresses pancreatic tumorigenesis

Clausen TM, Weiss RJ, Tremblay JR et al. · The Journal of clinical investigation 2025 · PMID 40924474 · doi:10.1172/JCI184172

This dataset

Open GSE270542 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 GSE270542_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 PRJNA1127467 and SRA study SRP515595. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 40924474) ↗

Study design

10 × Tumor, HS3ST1 KO, vs 8 × Tumor, WT,

Supports a between-group comparison across 18 samples.

How we read this: 2 replicated groups read from 18 sample titles; they account for 18 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

GSM8346377 Tumor, HS3ST1 KO, rep 1 Tumor, HS3ST1 KO,
GSM8346378 Tumor, HS3ST1 KO, rep 2 Tumor, HS3ST1 KO,
GSM8346379 Tumor, HS3ST1 KO, rep 3 Tumor, HS3ST1 KO,
GSM8346380 Tumor, WT, rep 1 Tumor, WT,
GSM8346381 Tumor, HS3ST1 KO, rep 4 Tumor, HS3ST1 KO,
GSM8346382 Tumor, HS3ST1 KO, rep 5 Tumor, HS3ST1 KO,
GSM8346383 Tumor, HS3ST1 KO, rep 6 Tumor, HS3ST1 KO,
GSM8346384 Tumor, WT, rep 2 Tumor, WT,
GSM8346385 Tumor, HS3ST1 KO, rep 7 Tumor, HS3ST1 KO,
GSM8346386 Tumor, WT, rep 3 Tumor, WT,
GSM8346387 Tumor, WT, rep 4 Tumor, WT,
GSM8346388 Tumor, WT, rep 5 Tumor, WT,
GSM8346389 Tumor, HS3ST1 KO, rep 8 Tumor, HS3ST1 KO,
GSM8346390 Tumor, HS3ST1 KO, rep 9 Tumor, HS3ST1 KO,
GSM8346391 Tumor, HS3ST1 KO, rep 10 Tumor, HS3ST1 KO,
GSM8346392 Tumor, WT, rep 6 Tumor, WT,
GSM8346393 Tumor, WT, rep 7 Tumor, WT,
GSM8346394 Tumor, WT, rep 8 Tumor, WT,

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Metadata from NCBI GEO, cached and refreshed periodically — the NCBI page above is authoritative. Downloads link straight to NCBI/ENA; nothing is proxied through BioTransfer.