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Prolonged KRAS-MAPK Inhibition Induces Interferon-mediated Epithelial-to-Mesenchymal Transition and Reveals Therapeutic Opportunities.

GSE303051 Homo sapiens (human) RNA-seq (gene expression) 30 samples Submitted 2026/03/25 Platform GPL21290
At a glance

RNA-seq (gene expression) · human · 30 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
Homo sapiens (human)
Topic
Pancreatic cancerThis series is part of our curated briefing on it.
Samples
30 samples: 10 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
Prolonged KRAS-MAPK Inhibition Induces Interferon Signaling That Promotes Cell State Transition and Confers Therapeutic VulnerabilitiesCancer research · 2026
Summary (written by the submitters)
Direct targeting of KRAS to inhibit the MAPK cascade is poised to transform the therapeutic landscape of pancreatic ductal adenocarcinoma (PDAC). However, analyses of PDAC samples from patients treated with KRASG12C inhibitors have revealed secondary mutations restoring MAPK signaling and promoting epithelial-to-mesenchymal transition (EMT) as key mechanisms of acquired resistance.
Read the full summary ↓
Here, we show that human PDAC specimens and patient-derived cell lines treated with the ERK inhibitor ulixertinib display upregulation of EMT-associated and inflammatory gene programs, particularly those linked to the interferon response. Using the GeneRep-nSCORE computational framework to reconstruct and rank regulatory networks enriched in ERKi and KRASi-resistant PDAC cells, we identified TRIM22, an interferon-inducible E3 ubiquitin ligase, as a critical mediator of EMT and treatment resistance. Mechanistically, TRIM22 promotes proteasomal degradation of IκBα, leading to activation of NF-κB signaling, a known driver of EMT. Notably, we identify TACSTD2, encoding Trophoblast Cell Surface Antigen 2 (TROP2), as an NF-κB target gene upregulated following EMT. Functionally, combining ulixertinib or the KRAS inhibitor MRTX1133 with the TROP2-directed antibody-drug conjugate sacituzumab govitecan significantly suppressed the growth of PDAC patient-derived xenografts. Together, our work identifies TRIM22 as a molecular link between interferon signaling and EMT and reveals TROP2 as a druggable vulnerability to sustain the therapeutic efficacy of KRAS-MAPK pathway inhibitors.
Published in
Prolonged KRAS-MAPK Inhibition Induces Interferon Signaling That Promotes Cell State Transition and Confers Therapeutic Vulnerabilities
Bulle A, Chen Y, Li H et al. · Cancer research 2026 · PMID 42008116 · doi:10.1158/0008-5472.CAN-25-4114
This dataset
Open GSE303051 in finder → Find more human RNA-seq datasets → Pancreatic cancer landscape →
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 GSE303051_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 PRJNA1293409 and SRA study SRP601840. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 42008116) ↗
Study design
10 conditions, mostly in triplicate
pa01c_vehicle ×3 pa01c_g12di ×3 Pa03c_Cont ×3 Pa03c_MRTX11 ×3 Pa014c_Cont ×3 Pa014c_MRTX11 ×3 HPAC_Cont ×3 HPAC_MRTX11 ×3 +2 more

Supports a between-group comparison across 30 samples.

How we read this: 10 replicated groups read from 30 sample titles; they account for 30 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
More Pancreatic cancer datasets

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