Abstract |
Basic, clinical and translational metabolic researches in cancer area have been extensively tried to discover and develop novel cancer metabolism drugs. Since tumor cells have metabolic dependencies that distinguish them from their normal counterparts, targeted inhibition of these metabolic dependencies is considered a promising therapeutic strategy against cancer. For example the representative cancer metabolism is that cancer cells exhibit profound metabolic alterations by choosing aerobic glycolysis to metabolize glucose to lactate regardless of the presence of adequate oxygen, although normal cells which mainly utilize glucose by using mitochondrial oxidative phosphorylation to generate ATP. In this review, we focus on several important oncogenes and enzymes, whose alterations have contributed extensively to the metabolic phenotype of cancer cells, with an emphasis on the therapeutic targets.
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Authors | Hideki Makinoshima, Satoshi Owada, Hiroyasu Esumi |
Journal | Nihon rinsho. Japanese journal of clinical medicine
(Nihon Rinsho)
Vol. 73
Issue 8
Pg. 1296-301
(Aug 2015)
ISSN: 0047-1852 [Print] Japan |
PMID | 26281681
(Publication Type: Journal Article, Review)
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Chemical References |
- Antineoplastic Agents
- Lactates
- Adenosine Triphosphate
- Isocitrate Dehydrogenase
- Proto-Oncogene Proteins c-akt
- TOR Serine-Threonine Kinases
- Glucose
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Topics |
- Adenosine Triphosphate
(metabolism)
- Animals
- Antineoplastic Agents
- Drug Discovery
- Glucose
(metabolism)
- Glycolysis
(genetics)
- Humans
- Isocitrate Dehydrogenase
(genetics)
- Lactates
(metabolism)
- Mice
- Mitochondria
(metabolism)
- Molecular Targeted Therapy
- Mutation
- Neoplasms
(enzymology, genetics, metabolism, therapy)
- Oxidation-Reduction
- Phosphatidylinositol 3-Kinases
(physiology)
- Phosphorylation
- Proto-Oncogene Proteins c-akt
(physiology)
- Signal Transduction
(physiology)
- TOR Serine-Threonine Kinases
(physiology)
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