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

摘要: The monocyte-macrophage lineage shows a high degree of diversity and plasticity. Once they infiltrate tissues, may acquire two main functional phenotypes, being known as the classically activated type 1 macrophages (M1) alternative 2 (M2). M1 phenotype can be induced by bacterial products interferon-γ exerts cytotoxic effect on cancer cells. Conversely, alternatively M2 is Il-4/IL13 promotes tumor cell growth vascularization. Although receptor for advanced glycation end-products (RAGE) engagement in has been reported several groups to promote inflammation, nothing about functionality RAGE macrophages. In current study, we demonstrate that equally expressed both macrophage phenotypes activation high-mobility group protein box1 (HMGB1) protumoral activities MKN45 cells co-cultured with treated HMGB1 at different times displayed higher invasive abilities. Additionally, conditioned medium from HMGB1-treated angiogenesis vitro. RAGE-targeting knockdown abrogates these activities. Overall, present findings suggest contribute, RAGE-dependent mechanism, phenotype.