{"database":"iProX","file_versions":[],"scores":null,"additional":{"omics_type":["Proteomics"],"submitter":["Debing Xiang"],"species":["Homo Sapiens"],"full_dataset_link":["http://www.iprox.org/page/project.html?id=IPX0017559000"],"submitter_email":["xdb86@cqu.edu.cn"],"submitter_affiliation":["Jiangjin Hospital of Chongqing University"],"sample_protocol":[""],"repository":["iProX"],"data_protocol":[""],"additional_accession":[]},"is_claimable":false,"name":"ECM1/SQSTM1 Axis Remodels Colorectal Cancer Immune Microenvironment via CXCL1-CXCR2-Dependent Neutrophil Recruitment and NETosis","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.","dates":{"publication":"Mon Jun 01 00:00:00 BST 2026"},"accession":"PXD079113","cross_references":{"TAXONOMY":["9606"]}}