Fig. 7: Proposed model for the role of CXCL5 in gastric cancer metastasis.

High level of CXCL5 in tumor microenvironment promotes GC metastasis by enhancing GC cell migration and invasion through the induction of EMT. CXCL5 exerts these effects by two mechanisms: (1) CXCL5 directly activates ERK signaling pathway in GC cells to upregulate Snail expression; (2) CXCL5 induces pro-tumor activation of neutrophils via ERK and p38 signaling pathways, which leads to the release of increased levels of inflammatory factors (e.g, IL-6 and IL-23), subsequently enhancing the metastatic potential of gastric cancer cells.