Angiogenesis is a critical process for cancer metastasis [32–34], and M2 macrophages have been reported to facilitate cancer angiogenesis [35, 36], which were verified by our results that M2-CM promoted tube formation abilities in HUVECs, which were abrogated by both silencing VEGF in the M2-CM and deletion of VEGFR in HUVECs (Supplementary Figure S4A, B), suggesting that M2 macrophages secreted VEGF, which interacted with VEGFR to activate its downstream signals and eventually facilitate tumor angiogenesis. Here, KDR is linked to neoplasm.