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WDR82 suppresses breast cancer progression by inhibiting ERK-driven chemokine expression and neutrophil infiltration

GSE325774 Mus musculus (mouse) RNA-seq (gene expression) 9 samples Submitted 2026/06/25 Platform GPL17021
At a glance

RNA-seq (gene expression) · mouse · 9 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
9 samples: 3 × p2 vs 3 × k28 vs 3 × k49Groups 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
WDR82 suppresses breast cancer progression by inhibiting ERK-driven chemokine expression and neutrophil infiltrationInternational journal of biological sciences · 2026
Summary (written by the submitters)
Elucidating tumor-intrinsic mechanisms that drive immune evasion and shape an immunosuppressive tumor microenvironment (TME) is essential for overcoming resistance to cancer immunotherapy and developing novel therapeutic strategies. WDR82, a member of the WD-40 protein family, exhibits context-dependent regulation of cancer, yet its role in breast cancer and its influence on the immunosuppressive TME remain undefined.
Read the full summary ↓
Here we identify WDR82 as a critical tumor suppressor that governs immune surveillance by restraining the ERK–chemokine–neutrophil axis. WDR82 expression is downregulated in human breast cancer and correlates with poor prognosis.Using orthotopic models, we uncover a functional paradox: while Wdr82 deficiency suppresses tumor cell proliferation in vitro, it accelerates tumor growth in vivo exclusively in immunocompetent hosts, driving enhanced neutrophil infiltration and CD8⁺ T cell exhaustion. Mechanistically, WDR82 directly binds MEK1/2, disrupting c-RAF-MEK assembly and restraining ERK activation. Loss of Wdr82 relieves this inhibition, driving ERK-dependent production of CXCL2 and CXCL7, the key neutrophil chemoattractants that promote CXCR2-mediated recruitment. Neutrophil depletion abolishes the tumor-promoting effect of Wdr82 deficiency, confirming the functional dependency on this axis. Importantly, intratumoral delivery of WDR82-expressing adenovirus reverses neutrophil accumulation, alleviates T cell exhaustion, and suppresses tumor progression. Our findings uncover a previously unrecognized mechanism by which WDR82 links tumor-intrinsic signaling to TME remodeling, establishing a promising therapeutic strategy for breast cancer through targeting the ERK–chemokine–neutrophil axis.
Published in
WDR82 suppresses breast cancer progression by inhibiting ERK-driven chemokine expression and neutrophil infiltration
Yu Q, Yang J, Lu F et al. · International journal of biological sciences 2026 · PMID 42328439 · doi:10.7150/ijbs.135015
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 GSE325774_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 PRJNA1441595 and SRA study SRP686026. Searching any of these in the dataset finder brings you back here.

Study design
3 × p2 vs 3 × k28 vs 3 × k49

Supports a between-group comparison across 9 samples.

How we read this: 3 replicated groups read from 9 sample titles; they account for 9 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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