http://www.cnr.it/ontology/cnr/individuo/prodotto/ID311224

PTX3 Is an Extrinsic Oncosuppressor Regulating Complement-Dependent Inflammation in Cancer. (Articolo in rivista)

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PTX3 Is an Extrinsic Oncosuppressor Regulating Complement-Dependent Inflammation in Cancer. (Articolo in rivista) (literal)

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Bonavita E, Gentile S, Rubino M, Maina V, Papait R, Kunderfranco P, Greco C, Feruglio F, Molgora M, Laface I, Tartari S, Doni A, Pasqualini F, Barbati E, Basso G, Galdiero MR, Nebuloni M, Roncalli M, Colombo P, Laghi L, Lambris JD, Jaillon S, Garlanda C, Mantovani A. (2015)
PTX3 Is an Extrinsic Oncosuppressor Regulating Complement-Dependent Inflammation in Cancer.
in Cell (Cambridge); Cell Press, Cambridge (Stati Uniti d'America)
(literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori

Bonavita E, Gentile S, Rubino M, Maina V, Papait R, Kunderfranco P, Greco C, Feruglio F, Molgora M, Laface I, Tartari S, Doni A, Pasqualini F, Barbati E, Basso G, Galdiero MR, Nebuloni M, Roncalli M, Colombo P, Laghi L, Lambris JD, Jaillon S, Garlanda C, Mantovani A. (literal)

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1Humanitas Clinical and Research Center, Rozzano (Milan) 20089, Italy. 2Humanitas Clinical and Research Center, Rozzano (Milan) 20089, Italy; Institute of Genetics and Biomedical Research, National Research Council, Rozzano (Milan) 20089, Italy. 3Pathology Unit, L. Sacco Department of Clinical Sciences, University of Milan, Milan 20157, Italy. 4Department of Pathology and Laboratory Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. 5Humanitas Clinical and Research Center, Rozzano (Milan) 20089, Italy. Electronic address: cecilia.garlanda@humanitasresearch.it. 6Humanitas Clinical and Research Center, Rozzano (Milan) 20089, Italy; Humanitas University, Rozzano (Milan) 20089, Italy. Electronic address: alberto.mantovani@humanitasresearch.it. (literal)

Titolo

PTX3 Is an Extrinsic Oncosuppressor Regulating Complement-Dependent Inflammation in Cancer. (literal)

Abstract

PTX3 is an essential component of the humoral arm of innate immunity, playing a nonredundant role in resistance against selected microbes and in the regulation of inflammation. PTX3 activates and regulates the Complement cascade by interacting with C1q and with Factor H. PTX3 deficiency was associated with increased susceptibility to mesenchymal and epithelial carcinogenesis. Increased susceptibility of Ptx3(-/-) mice was associated with enhanced macrophage infiltration, cytokine production, angiogenesis, and Trp53 mutations. Correlative evidence, gene-targeted mice, and pharmacological blocking experiments indicated that PTX3 deficiency resulted in amplification of Complement activation, CCL2 production, and tumor-promoting macrophage recruitment. PTX3 expression was epigenetically regulated in selected human tumors (e.g., leiomyosarcomas and colorectal cancer) by methylation of the promoter region and of a putative enhancer. Thus, PTX3, an effector molecule belonging to the humoral arm of innate immunity, acts as an extrinsic oncosuppressor gene in mouse and man by regulating Complement-dependent, macrophage-sustained, tumor-promoting inflammation. (literal)

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