Stat3 mediates myeloid cell-dependent tumor angiogenesis in mice.

摘要: The underlying molecular mechanisms that cause immune cells, mediators of our defense system, to promote tumor invasion and angiogenesis remain incompletely understood. Constitutively activated Stat3 in cells has been shown angiogenesis. Therefore, we sought determine whether activation tumor-associated inflammatory a similar function. We found signaling mediates multidirectional crosstalk among myeloid the stroma, ECs contributes mice. Myeloid-derived suppressor macrophages isolated from mouse tumors displayed induced an vitro tube formation assay via induction angiogenic factors, including VEGF bFGF. Stat3-regulated factors produced by both tumor-derived also constitutive endothelium, inhibiting substantially reduced factor-induced endothelial migration formation. In vivo assays demonstrated requirement for Our results indicate that, virtue ability upregulate expression activate ECs,