vegf111b

VEGF111b is a novel, naturally occurring C-terminal splice variant of VEGF-A in the VEGFxxxb family, induced by genotoxic agents such as mitomycin C, and has potent **anti-angiogenic** and **anti-tumor** properties. It inhibits angiogenesis and tumor growth by targeting the vascular endothelial growth factor receptor 2 (**VEGF-R2**, also known as KDR/Flk-1) and blocking its phosphorylation and downstream signaling pathways, namely the PI3K-Akt and ERK1/2 pathways. Overexpression of VEGF111b has been demonstrated to inhibit proliferation, migration, tube formation, and colony formation in ovarian cancer cells, induce S phase cell cycle arrest, and restrict in vivo tumor growth and microvessel density. VEGF111b acts similarly to VEGF165b—another anti-angiogenic VEGF-A isoform—but is induced specifically in response to DNA damage. Key mechanistic features include reduced VEGF-R2 tyrosine phosphorylation, reduced CD31-marked microvessel density, and a lack of binding to neuropilin-1 due to its unique C-terminal sequence[1][3][4].

Other names

VEGF111bVEGF-111bVEGF 111b