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Deletion of Egfr in myeloid cells counteracts an immuno-suppressive tumor microenvironment in CRC

ABSTRACT: Analysis of Tumor-promoting role of Egfr+ myeloid cells in CRC by scRNAseq revealed that Egfr signaling in myeloid cells promote CRC development via increased T cell exhaustion.

ORGANISM(S): Mus musculus

PROVIDER: GSE279941 | GEO | 2026/06/17

REPOSITORIES: GEO

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Deletion of Egfr in myeloid cells counteracts an immuno-suppressive tumor microenvironment in CRC

Project description:Despite advances in metastatic colorectal cancer (mCRC) treatment, it remains the second-leading cause of cancer-related deaths, with limited therapeutic options. EGFR inhibition is a first-line treatment for mCRC without KRAS mutations, but resistance persists in some patients. Preclinical murine CRC models have shown that EGFR deletion in myeloid cells results in smaller tumors, while the presence of EGFR-positive myeloid cells correlate with poor survival in mCRC patients. However, the role of these cells in tumor progression remains unclear. In this study, we used preclinical mouse models, scRNA-seq, proteomics, and mCRC patient data to investigate the impact of EGFR expression in myeloid cells on the tumor microenvironment (TME) and explore its therapeutic potential. We demonstrate that EGFR deletion in myeloid cells of tumor-bearing CRC mice reduces tumor growth, while EGFR deletion in tumor cells alone has no therapeutic effect. EGFR disruption also decreases F4/80hi macrophages, particularly Spp1+ and C1qc+ subsets, and reduces inflammatory signaling like TGFβ, IFNγ, JAK/STAT in myeloid cells. This, in turn, affects their interaction with T cells, promoting a shift towards a less immunosuppressive TME. Additionally, we identify reduced immune checkpoint expression and thrombospondin-1 (Thbs1) as a myeloid-derived ligand interacting with T-cells. Validation in human CRC shows that high expression of EGFR and THBS1 correlates with poorer prognosis. These findings highlight EGFR signaling in myeloid cells as a key modulator of the TME and suggest targeting EGFR in specific myeloid subsets could improve CRC treatment strategies.

2026-06-08 | PXD058770 | Pride

Deletion of Egfr in myeloid cells counteracts an immuno-suppressive tumor microenvironment in CRC

Project description:Deletion of Egfr in myeloid cells counteracts an immuno-suppressive tumor microenvironment in CRC

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Absence of EGFR signalling in granulocytic cells relieves immunosuppression sensitising CRC metastases to immune checkpoint therapy

Project description:Metastatic colorectal cancer (mCRC) is one of the deadliest cancers with very poor response to immune checkpoint blockade (ICB). Standard therapies employ chemotherapy combined with epidermal growth factor receptor (EGFR) blocking antibodies, which are only effective in a fraction of patients with RAS/RAF wild-type tumours. We have previously shown that EGFR deletion in myeloid cells of CRC, rather than in the cancer cells themselves, reduces tumour growth. Here, we investigate to which extent EGFR blockade in myeloid cells increases anti-tumour immunity thus sensitizing CRC to ICB. Using a syngeneic preclinical CRC liver metastasis model based on the transplantation of murine RAS mutant CRC organoids into mice lacking EGFR in myeloid cells, we observe a reduction in metastasis development accompanied by increased intratumoural T-cell infiltration. Importantly, we demonstrate that EGFR deletion reduces the capacity of granulocytic myeloid derived suppressor cells (G-MDSCSs) to suppress CD4+ T-cell proliferation. RNA-seq analysis of sorted MDSCs and T-cells uncovered an EGFR-dependent signature involved in immunosuppression, which in proficient-mismatch-repair (pMMR) CRC patients is associated with worse overall survival. Therapeutically, lifting immunosuppression by EGFR deletion in myeloid cells sensitised tumours to anti-PD-L1 treatment thus preventing liver metastasis development. These results imply that anti-EGFR therapies combined with ICB might be successful in preventing metastasis of RAS mutated CRC with high infiltration of suppressive EGFR+ myeloid cells.

2026-08-20 | GSE329741 | GEO

Single cell profiling of CRC primary tumors generated by the injection of AKTP mouse tumor organoid

Project description:The objective of this scRNAseq was to explore the heterogeneity between tumor epithelial CRC cells in our AKTP mouse models. We compared it to human datasets and found that mouse and human CRCs share similar tumor subpopulations.

2022-09-16 | E-MTAB-11284 | biostudies-arrayexpress

Single-cell Transcriptome Analysis Revealed that EGFR Mutation Leads to a Suppressive Tumor Immune Microenvironment in Lung Adenocarcinoma

Project description:We analyzed 40,799 single cells from nine samples and found that in EGFR-mutant LUAD, tumor cells generated an immunosuppressive microenvironment by releasing cytokines to attract suppressive immune cells such as myeloid-derived suppressor cells (MDSCs) directly or indirectly by interacting with macrophages, dendritic cells, or other cell types. By contrast, EGFR wild-type LUAD had a greater ability to recruit immunocompetent T cells such as TRMs and Th1 cells, thus driving a proinflammatory microenvironment.

2022-02-09 | GSE171145 | GEO

CRC

Project description:CRC Metagenome

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Liver metastases originating from 4 colorectal cancer patients (CRC-LM).

Project description:Using liver metastases from 4 colorectal cancer patients (CRC-LM), we explored one receptor: EGFR whose signaling triggers cell proliferation and is exacerbated in many tumors.

2023-06-14 | GSE217414 | GEO

Gene expression profile of 31 RAS/RAF-wild-type colorectal cancer (CRC) stem-cell (SC) spheroids and 7 FGFR-inhibitor resistant CSC-SC spheroids

Project description:This study investigated mechanisms of acquired resistance to FGFR inhibitor therapy in RAS/RAF–wild-type colorectal cancer (CRC). RNA sequencing (RNA-seq) data from 47 RAS/RAF-wild-type colorectal cancer stem-cell (CRC-SC) spheroid lines previously deposited under GSE205787 were integrated with newly generated RNA-seq data from 31 additional RAS/RAF-wild-type CRC-SC spheroid lines and seven FGFR inhibitor-resistant CRC-SC derivatives. The resistant derivatives were established from parental CRC-SC spheroid lines by continuous exposure to erdafitinib or futibatinib. Comparative transcriptomic analysis between matched parental and resistant lines revealed consistent upregulation of EGFR and downregulation of PTPROt, a truncated isoform of PTPRO, in resistant derivatives. Gene set enrichment analysis further indicated activation of EGFR-related signaling pathways in FGFR inhibitor-resistant spheroids. In addition, the integrated RNA-seq dataset comprising 78 RAS/RAF-wild-type CRC-SC lines was used to validate the inverse correlation between EGFR and PTPRO mRNA expression, supporting the involvement of PTPROt downregulation and EGFR pathway activation in acquired resistance to FGFR inhibition.

2026-06-09 | GSE333925 | GEO

Impact of myeloid cell specific deletion of EGFR on cardiac Cd11b+ non-myocyte gene expression

Project description:Epidermal Growth Factor Receptor (EGFR) is a critical factor regulating numerous aspects of cell biology. Though it is widely recognized as an oncogene, EGFR has been implicated in cardiovascular health, and has been shown to have unique cell specific roles in the heart. Macrophages and other myeloid cells play key roles in normal cardiac physiology and post injury pathological outcomes. Myeloid cell EGFR has been implicated in disease, though its role in the normal or failing heart has yet to be established. Here, we crossed EGFR floxed mice with LysM Cre transgenics to specifically delete EGFR in Cd11b+ myeloid cells. We then isolated non-cardiomyocytes and subject them to Cd11b microbeads and subsequent column concentration to obtain cardiac Cd11b+ non-myocyte myeloid cells. We used samples from floxed EGFR controls, and EGFR specific myeloid knockouts. In comparisson to control, myeloid EGFR knockouts had 763 differential transcripts when consdering p adjusted less than 0.05 and log2foldchange greater than absolute value 1.5.

2023-09-21 | GSE207686 | GEO

Absence of EGFR signalling in granulocytic cells relieves immunosuppression sensitising CRC metastases to immune checkpoint therapy

Project description:Absence of EGFR signalling in granulocytic cells relieves immunosuppression sensitising CRC metastases to immune checkpoint therapy

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