{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE348nnn/GSE348561/"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"omics_type":["Transcriptomics"],"species":["Mus musculus"],"gds_type":["Expression profiling by high throughput sequencing"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE348561"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"PLA2G2E is an inducer of IL-1B and CXCL2","description":"The immunosuppressive tumor microenvironment (TME) limits the efficacy of antitumor immune responses. Myeloid cells within the TME are thought to be educated to establish this immunosuppressive milieu, although the underlying mechanisms remain incompletely understood. Here, we show that tumor cells reprogram myeloid cells to produce interleukin-1B (IL-1B) and CXC chemokine ligand 2 (CXCL2) through the phospholipase PLA2G2E. IL-1B and CXCL2 in turn fuel the immunosuppressive TME by recruiting myeloid-derived suppressor cells (MDSCs). Targeting PLA2G2E promotes tumor clearance in mice. Together, these findings identify PLA2G2E as a mediator of tumor cell-myeloid cell communication and define the major sources of IL-1B and CXCL2 in the TME, highlighting PLA2G2E as a potential therapeutic target in cancer.","dates":{"publication":"2026/10/02"},"accession":"GSE348561","cross_references":{"GSM":["GSM10075247","GSM10075246","GSM10075245","GSM10075244","GSM10075243","GSM10075242"],"GPL":["18480"],"GSE":["348561"],"taxon":["Mus musculus"]}}