肿瘤细胞的异常糖代谢  

Abnormal glycometabolism in tumor cells

作　　者：孙洁[1] 孟祥军[1] 

机构地区：[1]上海交通大学附属第一人民医院消化内科,200080

出　　处：《国际肿瘤学杂志》2013年第12期883-885,共3页Journal of International Oncology

基　　金：国家自然科学基金（81272745）

摘　　要：肿瘤细胞糖代谢异常与多种机制有关，如缺氧诱导因子（HIF）的参与可激活糖酵解相关酶类，有利于肿瘤细胞采取糖酵解方式获能；线粒体功能低下或数量减少可一定程度抑制葡萄糖氧化磷酸化途径；某些癌基因的激活及抑癌基因的失活也参与调节线粒体氧化呼吸链及糖酵解相关酶类，从而影响糖代谢过程；肿瘤细胞氧化磷酸化的相关酶类合成受到抑制等。此外，糖代谢异常对肿瘤细胞的生长、侵袭和转移具有重要作用。The abnormal glucose metabolism of tumor cells is associated with a variety of mechanisms. Hypoxia inducible factor （HIF） is able to activate the glycolytic enzymes, which is conducive to getting energy through glycolysis. The dysfunction or the depletion in numbers of mitochondria can inhibit the oxidative phos- phorylation pathway of glucose to some extent. The activation of oncogenes and the inactivation of tumor sup- pressor genes are also involved in the regulation of mitochondrial respiratory chain and glycolytic enzymes, thus affecting the process of glucose metabolism. Compared with normal cells, the synthesis of oxidative phosphoryla- tion enzymes is inhibited in cancer cells. In addition, the abnormal glucose metabolism plays an important role in the growth, invasion and metastasis of tumor cells.

关 键 词：糖酵解 线粒体 肿瘤 缺氧诱导因子 

分 类 号：R730.23[医药卫生—肿瘤]