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Elucidating the impact of KRAS Gly12 mutants on homeostasis and tumorigenesis in the colonic epithelium

GSE301459 Mus musculus (mouse) RNA-seq (gene expression) 24 samples Submitted 2025/07/02 Platform GPL19057
At a glance

RNA-seq (gene expression) · mouse · 24 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
24 samples: 8 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)
KRAS mutations constitute one of the most prevalent and therapeutically relevant oncogenic drivers in human cancers. Clinical and epidemiological data suggest association between specific KRAS alleles, therapeutic response, and patient outcomes, however, direct experimental validation of these relationships has been limited. In this study, we employed genetically engineered mouse models (GEMMs) to investigate the differential impacts of three most common KRAS Gly12 mutations (KRASG12C, KRASG12D, and KRASG12V) in the context of intestinal homeostasis and tumorigenesis.
Read the full summary ↓
Although tumors developing from different KRAS Gly12 mutants exhibited no significant histological differences, their effects on survival outcomes of tumor bearing mice and therapeutic response displayed pronounced allele-specific differences. Our transcriptomic analyses revealed both allele-agnostic and allele specific transcriptional programs driven by KRAS Gly12 mutations in colon tumors. The allele-agnostic signature was characterized by enrichment of gene sets associated with MAPK signaling, receptor tyrosine kinase pathways, and immune-modulating pathways, compared to KRAS WT tumors. In contrast, allele-specific signature revealed unique OXPHOS pathway upregulation in KrasG12D tumors and marked enrichment of Notch and Wnt/-catenin signaling pathways in KrasG12C tumors. Inhibition of these pathways, in combination with KRASG12C inhibitor led to either addictive or synergistic reduction in tumor cell viability, in allele-specific manner. Collectively, these findings underscore the importance of understanding the distinct biological effects of KRAS Gly12 mutants on colon tumorigenesis and highlight the therapeutic relevance of allele specific signaling dependencies in colorectal cancer. These results provide key mechanistic insights and provide a foundation for the development of effective, allele-informed therapeutic strategies for KRAS mutant cancers.
This dataset
Open GSE301459 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 GSE301459_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 PRJNA1285271 and SRA study SRP597921. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 41963618) ↗
Study design
8 conditions, mostly in triplicate
Colonic epithelium from Fabp (Cre/+) mouse, ×3 Colonic epithelium from Fabp (Cre/+); Kras(LS… ×3 Colonic epithelium from Fabp (Cre/+); Kras(LS… ×3 Colonic epithelium from Fabp (Cre/+); Kras(LS… ×3 Colon tumor from Fabp (Cre/+); Apc (fl/+) mou… ×3 Colon tumor from Fabp (Cre/+); Apc (fl/+) mou… ×3 Colon tumor from Fabp (Cre/+); Apc (fl/+) mou… ×3 Colon tumor from Fabp (Cre/+); Apc (fl/+) mou… ×3

Supports a between-group comparison across 24 samples.

How we read this: 8 replicated groups read from 24 sample titles; they account for 24 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
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