The CXCL1 gene was initially identified by its constitutive overexpression in spontaneously transformed Chinese hamster fibroblasts, and the CXCL1 protein was originally purified as an autocrine growth factor from supernatants of a human melanoma cell line. CXCL1 is frequently overexpressed in many cancers, such as breast cancer, ovarian cancer, colorectal cancer, prostate cancer, and squamous cell carcinoma. CXCL1 is an ELR CXC chemokine, and it is structurally and functionally related to GRO2 (CXCL2), GRO3 (CXCL3), and interleukin-8 (CXCL8). CXCL1, CXCL3, and IL-8 bind to the CXCR2 receptor with CXCL1 (GROalpha) having the highest affinity. CXCL1 is crucial for the recruitment of neutrophils to inflammatory sites. In addition, CXCL1 has pleiotropic effects on cell proliferation, tumor angiogenesis, invasion, and metastasis. Thrombin enhances the secretion of CXCL1 from tumor cells, and these two molecules together induce vascular regulatory proteins and growth factors involved in angiogenesis; this parallels activity of VEGF, Ang-2, CD31, KDR, CXCR2, MMP1, and MMP2 in HUVEC cells. In addition, PGE2 stimulates expression of CXCL1 in human colorectal carcinoma cells through activation of an EGFR-MAPK. Furthermore, CXCL1 (secreted by CRC cells) induces endothelial cell migration and tube formation in vitro and in vivo. CXCL1 is induced by inflammatory cytokines such as IL-1 and TNF. In addition, IL-17A enhances expression of CXCL1 by prolonging the half-life of its constitutively unstable mRNA.