{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Araujo AM"],"funding":["European Research Council","Spanish Ministry of Economy and Competitiveness"],"pagination":["e148667"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8970678"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["132(7)"],"pubmed_abstract":["The tumor microenvironment (TME) is reprogrammed by cancer cells and participates in all stages of tumor progression. The contribution of stromal cells to the reprogramming of the TME is not well understood. Here, we provide evidence of the role of the cytokine oncostatin M (OSM) as central node for multicellular interactions between immune and nonimmune stromal cells and the epithelial cancer cell compartment. OSM receptor (OSMR) deletion in a multistage breast cancer model halted tumor progression. We ascribed causality to the stromal function of the OSM axis by demonstrating reduced tumor burden of syngeneic tumors implanted in mice lacking OSMR. Single-cell and bioinformatic analysis of murine and human breast tumors revealed that OSM expression was restricted to myeloid cells, whereas"],"journal":["The Journal of clinical investigation"],"pubmed_title":["Stromal oncostatin M cytokine promotes breast cancer progression by reprogramming the tumor microenvironment."],"pmcid":["PMC8970678"],"funding_grant_id":["804236","PI15/00623,PI18/00458,CP18/00076","819242"],"pubmed_authors":["Pulido L","Rodriguez J","Lopez-Velazco JI","Viera C","Tzankov A","Araujo AM","Coleman N","Fernandez-Nogueira P","Abaurrea A","Flores JM","Caffarel MM","Manzano S","Rezola R","Jenkins L","Osorio-Querejeta I","Lawrie CH","Eppenberger-Castori S","Valdes-Mora F","Urruticoechea A","Carracedo A","Martin-Martin N","Isacke CM","Azcoaga P","Ferrari N","Gallego-Ortega D","Egia-Mendikute L","Alvarez-Lopez I","Palazon A","Bragado P","Calvo F"],"additional_accession":[]},"is_claimable":false,"name":"Stromal oncostatin M cytokine promotes breast cancer progression by reprogramming the tumor microenvironment.","description":"The tumor microenvironment (TME) is reprogrammed by cancer cells and participates in all stages of tumor progression. The contribution of stromal cells to the reprogramming of the TME is not well understood. Here, we provide evidence of the role of the cytokine oncostatin M (OSM) as central node for multicellular interactions between immune and nonimmune stromal cells and the epithelial cancer cell compartment. OSM receptor (OSMR) deletion in a multistage breast cancer model halted tumor progression. We ascribed causality to the stromal function of the OSM axis by demonstrating reduced tumor burden of syngeneic tumors implanted in mice lacking OSMR. Single-cell and bioinformatic analysis of murine and human breast tumors revealed that OSM expression was restricted to myeloid cells, whereas","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Apr","modification":"2026-05-31T13:02:03.658Z","creation":"2025-04-06T21:48:51.657Z"},"accession":"S-EPMC8970678","cross_references":{"pubmed":["35192545"],"doi":["10.1172/JCI148667"]}}