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wunavy

木虫 (初入文坛)

应助: 0 (幼儿园)
金币: 1576
帖子: 47
在线: 22小时
虫号: 1131540
注册: 2010-10-25
性别: GG
专业: 骨、关节、软组织退行性病

[求助] P53与肿瘤细胞有氧糖酵解/瓦伯格效应之间的关系

今天看了一篇摘要大致内容是：
p53突变后失去对葡萄糖-6-磷酸脱氢酶（磷酸戊糖途径的限速酶）的抑制作用，致使细胞磷酸戊糖途径代谢增强，而这一发现能解释肿瘤细胞发生的有氧糖酵解（瓦伯格效应）。
请问：磷酸戊糖途径产生的NADPH和5-磷酸核糖对细胞的糖酵解有什么影响
（5-磷酸核糖可转变为3-磷酸甘油醛和6-磷酸果糖，这应该是有氧氧化和糖酵解的共同通路）

文献标题：p53 regulates biosynthesis through direct inactivation of glucose-6-phosphate dehydrogenase
Cancer cells consume large quantities of glucose and primarily use glycolysis for ATP production, even in the presence of adequate oxygen 1,2. This metabolic signature (aerobic glycolysis or the Warburg effect) enables cancer cells to direct glucose to biosynthesis, supporting their rapid growth and proliferation 3,4. However, both causes of the Warburg effect and its connection to biosynthesis are not well understood. Here we show that the tumor suppressor p53, the most frequently mutated gene in human tumors, inhibits the pentose phosphate pathway 5. Via the PPP, p53 suppresses glucose consumption, NADPH production, and biosynthesis. The p53 protein binds to glucose-6-phosphate dehydrogenase (G6PD), the first and rate-limiting enzyme of the PPP, and prevents the formation of the active dimer（. Tumor-associated p53 mutants lack the G6PD-inhibitory activity. Therefore, enhanced PPP glucose flux due to p53 inactivation may increase glucose consumption and direct glucose toward biosynthesis in tumor cells.

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