Fig. 2.

VEGF-induced vascular permeability leads to the accumulation of ascites. Tumor cells secrete VEGF and chemokines such as MCP-1 that attract macrophages, which secrete additional VEGF. VEGF binds to its receptor on vascular endothelial cells in the peritoneal wall, leading to the activation of focal adhesion kinase (FAK). Activated FAK binds to the tail of the VE-cadherin that mediates endothelial cell–cell junctions and phosphorylates β-catenin, triggering its release which destabilizes these junctions [82]. The resulting increase in vascular permeability is a major contributor to ascites formation and accumulation