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Skewed signaling through the receptor for advanced glycation end-products alters the proinflammatory profile of tumor-associated macrophages

dc.contributor.authorRojas, Armando
dc.contributor.authorAraya, Paulina
dc.contributor.authorRomero, Jacqueline
dc.contributor.authorDelgado-López, Fernando
dc.contributor.authorGonzález-Bonet, Ileana
dc.contributor.authorAñazco-Oyarzún, Carolina
dc.contributor.authorPérez-Castro, Ramón
dc.date.accessioned2019-01-04T17:59:03Z
dc.date.available2019-01-04T17:59:03Z
dc.date.issued2018
dc.identifier.urihttp://repositorio.ucm.cl/handle/ucm/2061
dc.description.abstractTumors are complex tissues composed of variable amounts of both non-cellular components (matrix proteins) and a multitude of stromal cell types, which are under an active cross-talk with tumor cells. Tumor-associated macrophages (TAMs) are the major leukocyte population among the tumor-infiltrating immune cells. Once they are infiltrated into tumor stroma they undergo a polarized activation, where the M1 and M2 phenotypes represent the two extreme of the polarization heterogeneity spectrum. It is known that TAMs acquire a specific phenotype (M2), oriented toward tumor growth, angiogenesis and immune-suppression. A growing body of evidences supports the presence of tuning mechanisms in order to skew or restraint the inflammatory response of TAMs and thus forces them to function as active tumor-promoting immune cells. The receptor of advanced glycation end-products (RAGE) is a member of the immunoglobulin protein family of cell surface molecules, being activated by several danger signals and thus signaling to promote the production of many pro-inflammatory molecules. Interestingly, this receptor is paradoxically expressed in both M1 and M2 macrophages phenotypes. This review addresses how RAGE signaling has been drifted away in M2 macrophages, and thus taking advantage of the abundance of RAGE ligands at tumor microenvironment, particularly HMGB1, to reinforce the supportive M2 macrophages strategy to support tumor growth.es_CL
dc.language.isoenes_CL
dc.rightsAtribución-NoComercial-SinDerivadas 3.0 Chile*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/3.0/cl/*
dc.sourceCancer Microenvironment, 11(2-3), 97-105es_CL
dc.subjectTumor microenvironmentes_CL
dc.subjectMacrophage polarizationes_CL
dc.subjectAlarminses_CL
dc.subjectTumor associated macrophageses_CL
dc.titleSkewed signaling through the receptor for advanced glycation end-products alters the proinflammatory profile of tumor-associated macrophageses_CL
dc.typeArticlees_CL
dc.ucm.facultadFacultad de Medicinaes_CL
dc.ucm.indexacionScopuses_CL
dc.ucm.urisibib2.ucm.cl:2048/login?url=https://link.springer.com/article/10.1007/s12307-018-0214-4es_CL
dc.ucm.doidoi.org/10.1007/s12307-018-0214-4es_CL


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Atribución-NoComercial-SinDerivadas 3.0 Chile
Excepto si se señala otra cosa, la licencia de la publicación se describe como Atribución-NoComercial-SinDerivadas 3.0 Chile