J Cancer 2017; 8(17):3430-3440. doi:10.7150/jca.21125

Review

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

Li Yu1✉*, Xun Chen2*, Xueqi Sun1, Liantang Wang 1, Shangwu Chen3✉

1. Department of Pathology, the First Affiliated Hospital, Sun Yat-sen University, Guangzhou 510080, People's Republic of China;
2. Guanghua School and Hospital of Stomatology, Sun Yat-sen University, Guangzhou 510055, People's Republic of China;
3. State Key Laboratory for Biocontrol, Guangdong Key Laboratory of Pharmaceutical Functional Genes, Key Laboratory of Gene Engineering of the Ministry of Education, Department of Biochemistry, School of Life Sciences, Sun Yat-sen University, Guangzhou 510275, People's Republic of China.
* The two authors contributed equally to this work.

Abstract

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.

Keywords: the Warburg effect, reprogramming of glucose metabolism, aerobic glycolysis, tumor metabolism, glycolytic switch.

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How to cite this article:
Yu L, Chen X, Sun X, Wang L, Chen S. The Glycolytic Switch in Tumors: How Many Players Are Involved?. J Cancer 2017; 8(17):3430-3440. doi:10.7150/jca.21125. Available from http://www.jcancer.org/v08p3430.htm