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ER-phagy and proteostasis defects create a pre-malignant injury state in Kras-mediated tumourigenesis (RNA-Seq)

GSE274978 Mus musculus (mouse) RNA-seq (gene expression) 16 samples Submitted 2025/08/06 Platform GPL24247

At a glance

RNA-seq (gene expression) · mouse · 16 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: 16 samples: 8 × Pancreas, KC WT, Mouse vs 8 × Pancreas, KC HOM, MouseGroups 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 acinar cells are surprisingly resistant to pre-malignant transformation by the mutant Kras oncogene. Here, reporter mice show that an early, transcriptionally-mediated effect of Kras activation is downregulation of ER-phagy. Subsequently, stochastic failure of ER-phagy correlates with pre-malignant transdifferentiation into acinar-ductal metaplasia (ADM).

Read the full summary ↓

Genetic perturbation of ER-phagy, combined with proteomics and transcriptomics, reveals endogenous injury, micro-inflammation and ADM across the acinar epithelium. Phenotypically, this occurs alongside intra-acinar formation of distinctive insoluble aggregates of ER proteins, including the injury marker REG3B. Mechanistically, REG3B is shown to bind to the ER-phagy receptor CCPG1 to facilitate degradation. Strikingly, spatial transcriptomics shows that oncogenic Kras also drives this cell state in a highly stochastic fashion, again characterised by protein aggregation, partial ductal identity, evidence of injury and propensity for ADM. Importantly, expression of insoluble mutant REG3B shows that protein aggregate formation directly engenders this state. Pancreatic cancer can thus arise from stochastic proteostatic defects that are both made probable by, and co-operate with, oncogenic Kras.

This dataset

Open GSE274978 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 GSE274978_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 PRJNA1148669 and SRA study SRP526729. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗

Study design

8 × Pancreas, KC WT, Mouse vs 8 × Pancreas, KC HOM, Mouse

Supports a between-group comparison across 16 samples.

How we read this: 2 replicated groups read from 16 sample titles; they account for 16 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

GSM8463342 Pancreas, KC WT, Mouse 1 Pancreas, KC WT, Mouse
GSM8463343 Pancreas, KC HOM, Mouse 1 Pancreas, KC HOM, Mouse
GSM8463344 Pancreas, KC HOM, Mouse 2 Pancreas, KC HOM, Mouse
GSM8463345 Pancreas, KC WT, Mouse 2 Pancreas, KC WT, Mouse
GSM8463346 Pancreas, KC HOM, Mouse 3 Pancreas, KC HOM, Mouse
GSM8463347 Pancreas, KC WT, Mouse 3 Pancreas, KC WT, Mouse
GSM8463348 Pancreas, KC WT, Mouse 4 Pancreas, KC WT, Mouse
GSM8463349 Pancreas, KC HOM, Mouse 4 Pancreas, KC HOM, Mouse
GSM8463350 Pancreas, KC WT, Mouse 5 Pancreas, KC WT, Mouse
GSM8463351 Pancreas, KC WT, Mouse 6 Pancreas, KC WT, Mouse
GSM8463352 Pancreas, KC HOM, Mouse 5 Pancreas, KC HOM, Mouse
GSM8463353 Pancreas, KC HOM, Mouse 6 Pancreas, KC HOM, Mouse
GSM8463354 Pancreas, KC WT, Mouse 7 Pancreas, KC WT, Mouse
GSM8463355 Pancreas, KC WT, Mouse 8 Pancreas, KC WT, Mouse
GSM8463356 Pancreas, KC HOM, Mouse 7 Pancreas, KC HOM, Mouse
GSM8463357 Pancreas, KC HOM, Mouse 8 Pancreas, KC HOM, Mouse

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GSE274979 ER-phagy and proteostasis defects create a pre-malignant injury state in Kras-mediated tumourigenesis (Spatial transcriptomics) 95 samples shares tumourigenesis, pre-malignant, kras-mediated, proteostasis, er-phagy, defects, create
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GSE296350 Fli1 inhibits proteostasis during nutrient stress to limit NK cell persistence in solid tumors [RNA-Seq_Mouse] 5 samples shares proteostasis, rna-seq
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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.