The Glycolytic Switch in Tumors: How Many Players Are Involved?

被引:164
作者
Yu, Li [1 ]
Chen, Xun [2 ]
Sun, Xueqi [1 ]
Wang, Liantang [1 ]
Chen, Shangwu [3 ]
机构
[1] Sun Yat Sen Univ, Affiliated Hosp 1, Dept Pathol, Guangzhou 510080, Guangdong, Peoples R China
[2] Sun Yat Sen Univ, Guanghua Sch & Hosp Stomatol, Guangzhou 510055, Guangdong, Peoples R China
[3] Sun Yat Sen Univ, Guangdong Key Lab Pharmaceut Funct Genes, Dept Biochem,Key Lab Gene Engn, Sch Life Sci,State Key Lab Biocontrol,Minist Educ, Guangzhou 510275, Guangdong, Peoples R China
来源
JOURNAL OF CANCER | 2017年 / 8卷 / 17期
基金
中国国家自然科学基金;
关键词
the Warburg effect; reprogramming of glucose metabolism; aerobic glycolysis; tumor metabolism; glycolytic switch; STIMULATES AEROBIC GLYCOLYSIS; REGULATES GLUCOSE-METABOLISM; HISTONE DEACETYLASE SIRT6; TARGETING HEXOKINASE 2; OVARIAN-CANCER CELLS; PYRUVATE-KINASE; UP-REGULATION; PANCREATIC-CANCER; MITOCHONDRIAL RESPIRATION; SUPPRESSES GLYCOLYSIS;
D O I
10.7150/jca.21125
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Reprogramming of cellular metabolism is a hallmark of cancers. Cancer cells more readily use glycolysis, an inefficient metabolic pathway for energy metabolism, even when sufficient oxygen is available. This reliance on aerobic glycolysis is called the Warburg effect, and promotes tumorigenesis and malignancy progression. The mechanisms of the glycolytic shift in tumors are not fully understood. Growing evidence demonstrates that many signal molecules, including oncogenes and tumor suppressors, are involved in the process, but how oncogenic signals attenuate mitochondrial function and promote the switch to glycolysis remains unclear. Here, we summarize the current information on several main mediators and discuss their possible mechanisms for triggering the Warburg effect.
引用
收藏
页码:3430 / 3440
页数:11
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