Cancer cell metabolism: implications for therapeutic targets.
- Author:
Miran JANG
1
;
Sung Soo KIM
;
Jinhwa LEE
Author Information
1. Department of Biochemistry and Molecular Biology, Medical Science and Engineering Research Center for Bioreaction to Reactive Oxygen Species (BK-21) and Biomedical Science Institute, School of Medicine, Kyung Hee University, Seoul, Republic of Korea. sgsk
- Publication Type:Review ; Research Support, Non-U.S. Gov't
- Keywords:
aerobic glycolysis;
cancer;
metabolism;
Warburg effect
- MeSH:
Animals;
Antineoplastic Agents/*pharmacology/therapeutic use;
Carcinogenesis/drug effects/metabolism;
Glycolysis/*drug effects;
Humans;
Neoplasms/drug therapy/*metabolism
- From:Experimental & Molecular Medicine
2013;45(10):e45-
- CountryRepublic of Korea
- Language:English
-
Abstract:
Cancer cell metabolism is characterized by an enhanced uptake and utilization of glucose, a phenomenon known as the Warburg effect. The persistent activation of aerobic glycolysis in cancer cells can be linked to activation of oncogenes or loss of tumor suppressors, thereby fundamentally advancing cancer progression. In this respect, inhibition of glycolytic capacity may contribute to an anticancer effect on malignant cells. Understanding the mechanisms of aerobic glycolysis may present a new basis for cancer treatment. Accordingly, interrupting lactate fermentation and/or other cancer-promoting metabolic sites may provide a promising strategy to halt tumor development. In this review, we will discuss dysregulated and reprogrammed cancer metabolism followed by clinical relevance of the metabolic enzymes, such as hexokinase, phosphofructokinase, pyruvate kinase M2, lactate dehydrogenase, pyruvate dehydrogenase kinase and glutaminase. The proper intervention of these metabolic sites may provide a therapeutic advantage that can help overcome resistance to chemotherapy or radiotherapy.
