HMGB1 enhances the protumoral activities of M2 macrophages by a RAGE-dependent mechanism

dc.creatorRojas, Armando
dc.creatorDelgado-López, Fernando
dc.creatorPérez-Castro, Ramón
dc.creatorGonzález-Bonet, Ileana
dc.creatorRomero, Jacqueline
dc.creatorRojas, Israel
dc.creatorAraya, Paulina
dc.creatorMorales-Mejías, Erik
dc.creatorLlano, Jorge
dc.creatorAñazco-Oyarzún, Carolina
dc.date2017-10-03T17:54:25Z
dc.date2017-10-03T17:54:25Z
dc.date2016
dc.date.accessioned2019-11-20T15:07:48Z
dc.date.available2019-11-20T15:07:48Z
dc.identifierhttp://repositorio.ucm.cl:8080/handle/ucm/301
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/3032035
dc.descriptionThe monocyte-macrophage lineage shows a high degree of diversity and plasticity. Once they infiltrate tissues,they may acquire two main functional phenotypes, being known as the classically activated type 1 macrophages (M1) and the alternative activated type 2 macrophages (M2). The M1 phenotype can be induced by bacterial products and interferon-γ and exerts a cytotoxic effect on cancer cells. Conversely, the alternatively activated M2 phenotype is induced by Il-4/IL13 and promotes tumor cell growth and vascularization. Although receptor for advanced glycation endproducts (RAGE) engagement in M1 macrophages has been reported by several groups to promote inflammation, nothing is known about the functionality of RAGE in M2 macrophages. In the current study, we demonstrate that RAGE is equally expressed in both macrophage phenotypes and that RAGE activation by high-mobility group protein box1 (HMGB1) promotes protumoral activities of M2 macrophages. MKN45 cells co-cultured with M2 macrophages treated with HMGB1 at different times displayed higher invasive abilities. Additionally, conditioned medium from HMGB1-treated M2 macrophages promotes angiogenesis in vitro. RAGE-targeting knockdown abrogates these activities. Overall, the present findings suggest that HMGB1 may contribute, by a RAGE-dependent mechanism, to the protumoral activities of the M2 phenotype.
dc.languageen
dc.rightsAtribución-NoComercial-SinDerivadas 3.0 Chile
dc.rightshttp://creativecommons.org/licenses/by-nc-nd/3.0/cl/
dc.sourceTumor Biology, 37(3), 3321-3329
dc.subjectReceptor for advanced glycation end products
dc.subjectHMGB1
dc.subjectMacrophage polarization
dc.subjectTumor-associated macrophages
dc.titleHMGB1 enhances the protumoral activities of M2 macrophages by a RAGE-dependent mechanism
dc.typeArtículos de revistas


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