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

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...

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Bibliographic Details
Published in:Journal of Cancer 2017-01, Vol.8 (17), p.3430-3440
Main Authors: Yu, Li, Chen, Xun, Sun, Xueqi, Wang, Liantang, Chen, Shangwu
Format: Article
Language:English
Subjects:
Review
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Summary: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.
ISSN:1837-9664
1837-9664
DOI:10.7150/jca.21125