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正常细胞代谢所需能量主要由线粒体氧化磷酸化(OXPHOS)产生的ATP提供。与正常细胞不同,肿瘤细胞多通过糖酵解途径消耗更多的葡萄糖,并产生大量乳酸,却很少利用OXPHOS产能。但肿瘤细胞高糖酵解能量代谢表型的具体分子机制目前尚不完全明确,其高糖酵解活性可能涉及到糖酵解酶和葡萄糖转运蛋白过表达、呼吸链缺陷及线粒体DNA(mtDNA)易感于氧化应激等机制。本文就肿瘤细胞高糖酵解活性的基因和能量代谢调节机制的研究进展作一综述。
The energy required for normal cellular metabolism is provided primarily by ATP produced by mitochondrial oxidative phosphorylation (OXPHOS). Unlike normal cells, tumor cells often consume more glucose through the glycolytic pathway and produce more lactic acid, but seldom utilize OXPHOS capacity. However, the specific molecular mechanisms of the energy metabolism phenotype of tumor cells with high glycolysis are not yet fully understood. The high glycolysis activity may involve overexpression of glycolytic enzymes and glucose transporters, respiratory chain defects and mitochondrial DNA (mtDNA) Susceptible to oxidative stress and other mechanisms. This review summarizes the research progress on the mechanism of tumor cell hyperglycogenolytic regulation of gene and energy metabolism.