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Vascular endothelial growth inhibitor (VEGI), also known as TNFSF15 or TL1A, is an endogenous cytokine belonging to the tumor necrosis factor (TNF) superfamily. It is primarily produced by endothelial cells and functions as a potent autocrine inhibitor of angiogenesis. VEGI exerts its biological effects by signaling through receptors such as Death Receptor 3 (TNFRSF25) and interacting with the decoy receptor DcR3 (TNFRSF6B). In the context of oncology, VEGI has been shown to inhibit the proliferation, tube formation, and migration of vascular endothelial cells, thereby suppressing tumor-related vasculature and growth. Research in renal cell carcinoma (RCC) has demonstrated that VEGI expression is frequently downregulated in high-grade tumors, and its restoration via forced expression can significantly reduce tumor aggressiveness and microvessel density in preclinical models.
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