{"database":"ENA","file_versions":[],"scores":null,"additional":{"omics_type":["Genomics"],"center_name":["Fudan University"],"full_dataset_link":["https://www.ebi.ac.uk/ena/browser/view/PRJNA382567"],"scientific_name":["Mus musculus"],"tag":["xref:PubMed:30333314"],"long_description":["Molecular mechanisms underlying the cancer stroma in metastasis is largely unknown. Here we show that cancer-associated fibroblasts (CAFs) produce high levels of IL-33 that acted on tumor-associated macrophages (TAMs) to induce the M1 to M2 transition. Genome profiling of metastasis-related genes in the IL-33-stimulated TAMs showed a > 200-fold increase of metalloproteinase 9 (MMP9). Signaling analysis demonstrated the IL-33-ST2-NFkB-MMP9-laminin pathway that mediates cancer metastasis. In mouse and human fibroblast-rich pancreatic cancers, genetic deletion of IL-33, ST2 and MMP9 markedly blocked metastasis. Pharmacological inhibition of NFkB and MMP9 also blocked cancer metastasis. Deletion of IL-33, ST2 and MMP9 restored laminin, a key basement membrane component associated to tumor microvessels. Together, our data provide novel mechanistic insights on the IL-33-NFkB-MMP9-laminin axis that mediates the CAF-TAM-committed cancer metastasis. Thus, targeting the CAF-TAM-vessel interaction provides an outstanding therapeutic opportunity for cancer treatment. Overall design: Raw 264.7 monocytes are treated with or without 50 ng/ml IL-33 (n=3 samples/group)"],"repository":["ENA"],"additional_accession":[]},"is_claimable":false,"name":"Mus musculus","description":"Gene expression profile of RAW264.7 monocytes treated with or without IL-33","dates":{"last_updated":"2025-09-24","first_public":"2017-06-01"},"accession":"PRJNA382567","cross_references":{"GEO":["GSE97657"],"taxon":["10090"],"PubMed":["30333314"]}}