期刊
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
卷 20, 期 2, 页码 -出版社
MDPI
DOI: 10.3390/ijms20020238
关键词
hypoxia; HIF-1; glucose metabolism; cancer
资金
- Research Project on Development of New Drugs from Japan Agency for Medical Research and development (AMED) [17ak0101084h0001]
- Bilateral Joint Research Projects from Japan Society for the Promotion of Science (JSPS)
- MEXT, Japan [17H04261, 18KK0241, 18H04977, 16H01573, 18K15589]
- research grant programs of the Princess Takamatsu Cancer Research Fund
- Takeda Science Foundation
- Relay for Life Japan
- Ichiro Kanehara Foundation for the Promotion of Medical Sciences and Medical Care
- Uehara Memorial Foundation
- Kobayashi Foundation for Cancer Research
- Research Project on Development of New Drugs from AMED [17ak0101084h0001]
- JSPS, Japan [17J07699]
- Joint Usage Program of the Radiation Biology Center, Kyoto University
- Institute for Integrated Radiation and Nuclear Science, Kyoto University
- Grants-in-Aid for Scientific Research [18H04977, 17H04261, 16H01573, 18K15589, 18KK0241, 17J07699] Funding Source: KAKEN
Normal cells produce adenosine 5'-triphosphate (ATP) mainly through mitochondrial oxidative phosphorylation (OXPHOS) when oxygen is available. Most cancer cells, on the other hand, are known to produce energy predominantly through accelerated glycolysis, followed by lactic acid fermentation even under normoxic conditions. This metabolic phenomenon, known as aerobic glycolysis or the Warburg effect, is less efficient compared with OXPHOS, from the viewpoint of the amount of ATP produced from one molecule of glucose. However, it and its accompanying pathway, the pentose phosphate pathway (PPP), have been reported to provide advantages for cancer cells by producing various metabolites essential for proliferation, malignant progression, and chemo/radioresistance. Here, focusing on a master transcriptional regulator of adaptive responses to hypoxia, the hypoxia-inducible factor 1 (HIF-1), we review the accumulated knowledge on the molecular basis and functions of the Warburg effect and its accompanying pathways. In addition, we summarize our own findings revealing that a novel HIF-1-activating factor enhances the antioxidant capacity and resultant radioresistance of cancer cells though reprogramming of the glucose metabolic pathway.
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