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ECM1/SQSTM1 Axis Remodels Colorectal Cancer Immune Microenvironment via CXCL1-CXCR2-Dependent Neutrophil Recruitment and NETosis (scRNA-seq)

ABSTRACT: Extracellular matrix protein 1 (ECM1) has been implicated in tumorigenesis; however, its precise role in modulating the immunosuppressive tumor microenvironment (ITM) in colorectal cancer (CRC) remains inadequately elucidated.

ORGANISM(S): Mus musculus

PROVIDER: GSE334233 | GEO | 2026/06/08

REPOSITORIES: GEO

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ECM1/SQSTM1 Axis Remodels Colorectal Cancer Immune Microenvironment via CXCL1-CXCR2-Dependent Neutrophil Recruitment and NETosis (Spatial transcriptomics)

Project description:Extracellular matrix protein 1 (ECM1) has been implicated in tumorigenesis; however, its precise role in modulating the immunosuppressive tumor microenvironment (ITM) in colorectal cancer (CRC) remains inadequately elucidated.

2026-06-08 | GSE334234 | GEO

ECM1/SQSTM1 Axis Remodels Colorectal Cancer Immune Microenvironment via CXCL1-CXCR2-Dependent Neutrophil Recruitment and NETosis

Project description:In this study, we demonstrate that ECM1 derived from intestinal epithelial cells (IECs) serves as a critical driver of CRC progression. The deficiency of Ecm1 specifically in intestinal epithelial significantly suppresses both colitis-associated and spontaneous colorectal tumorigenesis in vivo. Through single-cell and spatial transcriptomic analyses, we reveal that ECM1 regulates neutrophil recruitment and activation within the tumor microenvironment (TME). Mechanistically, ECM1 functions as a scaffold protein that facilitates the interaction between SQSTM1 and RIP1, thereby initiating NF-κB-meditated CXCL1 secretion. This signaling pathway recruits neutrophils and induces the formation of neutrophils extracellular traps (NETs), creating an immune barrier that excludes CD8+ T cells. Notably, targeting ECM1 effectively mitigates neutrophil-mediated immunosuppression and reverses anti-PD-1 immunotherapy resistance in subcutaneous tumor-bearing mice.

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Transcriptome Sequencing Analysis of Human Colorectal Cancer Cell Lines After ECM1 Knockdown

Project description:To investigate the regulatory role of ECM1 in CCL20 expression in colorectal cancer, this study employed the human colorectal cancer SW620 cell line. Stable knockdown of ECM1 gene expression was achieved via shRNA, and single-cell transcriptome sequencing technology was used to systematically compare the transcriptomic differences between the ECM1 knockdown group (SW620-shECM1) and the negative control group (SW620-shNC). Sequencing analysis revealed that ECM1 knockdown significantly affected multiple signaling pathways, among which the TNF-α signaling pathway was notably activated, and the expression and activity of the key transcription factor JUNB underwent significant changes. Further mechanistic studies demonstrated that ECM1 regulates the transcription and expression of the downstream chemokine CCL20 by modulating the TNF-α/JUNB signaling axis. This study is the first to reveal the molecular mechanism by which ECM1 regulates CCL20 through the TNF-α-JUNB pathway in colorectal cancer at the single-cell level, providing a new perspective for understanding the role of ECM1 in the tumor microenvironment and immune regulation.

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Human melanoma cells over-express Extracellular Matrix 1 (ECM1) which is regulated in part by TFAP2C

Project description:Extracellular Matrix 1(ECM1) expression is increased in multiple tumor cell lines and primary cancers. Activator protein 2C (TFAP2C) is a potent regulator of ECM1 transcription. TFAP2C may contribute to the increased ECM1 expression noted in many cancers. This is the first report identifying the minimal promoter region of the human ECM1 gene and its regulation by TFAP2C Human A375 melanoma cells were assessed for mRNA and protein expression of ECM1. A mininal promoter region for ECM1 transactivation was identified. ECM1 expression was regulated in part by TFAP2C, and in ChIP-Seq experiments, TFAP2C was found to bind directly to the ECM1 gene in A375 melanoma cells and in MCF7 breast cancer cells.

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Expression data from Th2 cell of ECM1 KO mice vs WT mice

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Project description:Extracellular Matrix Protein-1 (ECM1) promotes tumorigenesis in multiple organs, but the mechanisms associated with the functions and putative receptors of ECM1 subtypes have yet to be systematically clarified. We found in this study that secretory ECM1a functions as an oncoprotein to induce tumorigenesis through binding of the Gly-Pro-Arg (GPR) motif to integrin aXb2 and activation of AKT/FAK/Rho/cytoskeletal signaling. Nonsecretory ECM1b binds to myosin to block myosin phosphorylation, thus preventing cytoskeletal signaling activation and tumorigenesis. Based on RNA sequencing, we further found that the heterogeneous nuclear ribonucleoprotein L-like (hnRNPLL) protein induced by ECM1a favors the alternative mRNA splicing of ECM1a to control ECM1-associated signaling and tumorigenesis. ATP binding cassette subfamily G member 1 (ABCG1) transduces ECM1a-integrin aXb2 interactive signaling to facilitate the phosphorylation of AKT/FAK/Rho/cytoskeletal molecules and to confer cisplatin resistance in cancer cells through upregulation of CD326-mediated cell stemness.

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