Vasohibin-2

Mechanism of Action

• Secreted by macrophages and tumor-infiltrating cells into the tumor microenvironment
• Stimulates endothelial cell migration and proliferation, promoting tumor vascularization
• Detyrosinates alpha-tubulin (same enzymatic activity as VASH1), but net cellular context drives pro-angiogenic outcome
• Upregulates VEGF-A expression in surrounding stromal cells
• High VASH2/VASH1 ratio in tumors correlates with increased microvessel density and poor prognosis

Research Findings

• VASH2 knockdown in tumor cell lines reduced xenograft tumor growth and vascularization in mice
• High VASH2 expression associated with poor survival in ovarian, hepatocellular, and pancreatic cancers
• VASH2 promotes epithelial-mesenchymal transition in cancer cells via TGF-beta pathway modulation
• VASH2 knockout mice show impaired corpus luteum angiogenesis, suggesting roles in reproductive biology
• Anti-VASH2 antibodies under preclinical development as anti-tumor vascular targeting agents

Research Protocols

• Research tool: siRNA or shRNA knockdown of VASH2 in cancer cell line experiments
• Recombinant VASH2 protein at 50-200 ng/mL to assess pro-angiogenic effects in vitro
• Anti-VASH2 neutralizing antibody at 10 mg/kg in mouse tumor models
• No clinical protocols; target for future anti-cancer drug development

Interactions

• SVBP: required co-factor for enzymatic activity and secretion
• VASH1: functional antagonist; balance of VASH1/VASH2 determines net angiogenic tone
• TGF-beta signaling: VASH2 amplifies TGF-beta-driven EMT and invasion

Safety Profile

Research target only. No human dosing data. VASH2 inhibition is the desired therapeutic goal, not administration of the protein.

Legal & Regulatory

Research target; no approved therapeutic