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Transcriptional profiling of tumor infiltrating neutrophils in a mouse model (MOC1) of oral cavity cancer

GSE309017 Mus musculus Expression profiling by high throughput sequencing 4 samples Submitted 2025/09/25 Platform GPL30172
Summary
Neutrophils are abundant in the tumor microenvironment and frequently acquire immunosuppressive phenotypes, yet the mechanisms driving this transition remain incompletely defined. To investigate the role of the transcription factor Egr1 and MEK signaling in neutrophil-mediated immune suppression, we performed single-cell RNA sequencing (scRNA-seq) of tumor-infiltrating neutrophils isolated from a syngeneic oral cavity cancer model (MOC1) in mice. This dataset comprises four experimental groups: Egr1 wild-type (WT) vs. Egr1 knockout (KO) and vehicle control vs. trametinib (MEK inhibitor) treatment. Comparative transcriptional profiling revealed that Egr1-deficient neutrophils fail to upregulate key immunosuppressive and pro-inflammatory effectors, including Osm, Ptgs2, and Il1b, in response to the tumor microenvironment. Conversely, trametinib-treated neutrophils displayed reduced expression of hypoxia- and MEK-driven transcriptional programs, including suppression of Osm, Ptgs2, Il1b, and the AP-1 transcription factor Junb.
Published in
Hypoxia-induced EGR1 remodels neutrophils to suppress antitumor immunity
Chang TG, Friedman J, Clavijo PE et al. · Science immunology 2025 · PMID 41385607 · doi:10.1126/sciimmunol.adz2273
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Direct links to NCBI, no account and no request form: the whole study as GSE309017_RAW.tar, processed values as the series matrix, the supplementary file directory, and per-sample supplementary files for any of the 4 samples. Raw sequencing reads are also available from ENA.

Also filed as BioProject PRJNA1333715 and SRA study SRP626266. Searching any of these in the dataset finder brings you back here.

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