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恶性实体肿瘤的生长必须依赖新生血管持续不断地为其提供营养和排泄代谢产物。血管内皮生长因子 (VEGF)有很强的促血管生成作用 ,对血管生成的关键环节即血管内皮细胞持续增殖具有直接作用。而野生型 P5 3抑制 VEGF的表达 ,突变型 P5 3则可以增加 VEGF的表达 [1 ,2 ] 。本实验
Malignant solid tumor growth must rely on neovascularization to provide continuous nutrition and excretion of metabolites. Vascular endothelial growth factor (VEGF) has a strong pro-angiogenic effect, a key component of angiogenesis, vascular endothelial cells continue to have a direct role in proliferation. However, wild-type P5 3 inhibited the expression of VEGF and mutant P5 3 increased the expression of VEGF [1,2]. this experiment