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dc.contributor.authorDrehmer, Daiana
dc.contributor.authorMesquita Luiz, J. P.
dc.contributor.authorHernandez, C. A. S.
dc.contributor.authorAlves-Filho, J. C.
dc.contributor.authorHussell, T.
dc.contributor.authorTownsend, Paul A
dc.contributor.authorMoncada, Salvador
dc.date.accessioned2022-08-01T09:07:00Z
dc.date.available2022-08-01T09:07:00Z
dc.date.issued2022en
dc.identifier.citationDrehmer D, Mesquita Luiz JP, Hernandez CAS, Alves-Filho JC, Hussell T, Townsend PA, et al. Nitric oxide favours tumour-promoting inflammation through mitochondria-dependent and -independent actions on macrophages. Vol. 54, Redox Biology. Elsevier BV; 2022. p. 102350.en
dc.identifier.pmid35660630en
dc.identifier.doi10.1016/j.redox.2022.102350en
dc.identifier.urihttp://hdl.handle.net/10541/625355
dc.description.abstractProduction of nitric oxide (NO) has been demonstrated in several malignancies, however its role remains not fully understood, specifically in relation to the metabolic and functional implications that it may have on immune cells participating in tumorigenesis. Here, we show that inducible NO synthase (iNOS) is expressed in cancers of the colon and the prostate, mainly by tumour cells, and NO generation is evidenced by widespread nitrotyrosine (NT) staining in tumour tissue. Furthermore, presence of NT is observed in the majority of tumour-associated macrophages (TAMs), despite low iNOS expression by these cells, suggesting that NO from the tumour microenvironment affects TAMs. Indeed, using a co-culture model, we demonstrate that NO produced by colon and prostate cancer cells is sufficient to induce NT formation in neighbouring macrophages. Moreover, exposure to exogenous NO promotes mitochondria-dependent and -independent changes in macrophages, which orientate their polarity towards an enhanced pro-inflammatory phenotype, whilst decreasing antigen-presenting function and wound healing capacity. Abrogating endogenous NO generation in murine macrophages, on the other hand, decreases their pro-inflammatory phenotype. These results suggest that the presence of NO in cancer may regulate TAM metabolism and function, favouring the persistence of inflammation, impairing healing and subverting adaptive immunity responses.en
dc.language.isoenen
dc.relation.urlhttps://dx.doi.org/10.1016/j.redox.2022.102350en
dc.titleNitric oxide favours tumour-promoting inflammation through mitochondria-dependent and -independent actions on macrophagesen
dc.typeArticleen
dc.contributor.departmentDivision of Cancer Sciences, Manchester Cancer Research Centre, Faculty of Biology, Medicine and Health, University of Manchester, Manchester, UKen
dc.identifier.journalRedox Biologyen
dc.description.noteen]
refterms.dateFOA2022-08-01T10:39:40Z


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