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Loss of rhomboid protease RHBDL4 delays tumour initiation in a mouse model of breast cancer

GSE314202 Mus musculus (mouse) RNA-seq (gene expression) 10 samples Submitted 2026/02/28 Platform GPL24247
At a glance

RNA-seq (gene expression) · mouse · 10 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
10 samples: 2 × MMTV-PyMT mammary tumour - RHBDL4 KO - Sample 990BT vs 2 × MMTV-PyMT mammary tumour - RHBDL4 WT - Sample 968BT vs 2 × MMTV-PyMT mammary tumour - RHBDL4 WT - Sample 1061BTGroups 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)
Despite advances in detection and treatment, breast cancer still claims more than 600,000 lives each year. Understanding the molecular pathways that initiate and sustain tumour growth is essential for improving patient outcomes. Among the regulators of these pathways are intramembrane proteases such RHBDL4, an intramembrane rhomboid serine protease.
Read the full summary ↓
RHBDL4 has been implicated in several cancers, including breast cancer, yet its precise role in tumour progression remains unclear. Using the MMTV-PyMT mouse model to investigate RHBDL4’s contribution to mammary tumourigenesis; we found that its genetic loss markedly delayed tumour onset, impeded early tumour growth, and suppressed AKT1 signalling and associated metabolic gene programs. Immunohistochemical analyses found RHBDL4 knockout mammary ducts exhibited reduced proliferative signalling and increased apoptotic signalling. In contrast, RHBDL4 loss had no detectable effect on metastasis or late-stage tumour progression, indicating that RHBDL4 functions primarily during the early phases of tumour development. These findings identify RHBDL4 as a regulator of early oncogenic transformation and reveal its temporally restricted role in mammary tumourigenesis.
This dataset
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.

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 GSE314202_RAW.tar (it can run to tens of gigabytes).

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.

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 PRJNA1390244 and SRA study SRP656083. Searching any of these in the dataset finder brings you back here.

Study design
2 × MMTV-PyMT mammary tumour - RHBDL4 KO - Sample 990BT vs 2 × MMTV-PyMT mammary tumour - RHBDL4 WT - Sample 968BT vs 2 × MMTV-PyMT mammary tumour - RHBDL4 WT - Sample 1061BT

Supports a between-group comparison across 6 samples.

How we read this: 3 replicated groups read from 10 sample titles; they account for 6 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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