CXCL1 and neoplasm: HUVEC tube formation was abolished by CXCR2 blockade in the conditioned media of HCT116 and HT29 cells (Figure 3E), indicating that the levels of CXCL1, CXCL2, and CXCL4 induced by GNA13 in CRC cells might promote tumor angiogenesis by binding with CXCR2 receptors on endothelial cells.