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논문 기본 정보

자료유형
학술저널
저자정보
Quangdon Tran (Chungnam National University) Hyunji Lee (Chungnam National University) Jisoo Park (Chungnam National University) Seon-Hwan Kim (Chungnam National University) Jongsun Park (Chungnam National University)
저널정보
한국독성학회 Toxicological Research Toxicological Research Vol.32 No.3
발행연도
2016.7
수록면
177 - 193 (17page)

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초록· 키워드

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After more than half of century since the Warburg effect was described, this atypical metabolism has been standing true for almost every type of cancer, exhibiting higher glycolysis and lactate metabolism and defective mitochondrial ATP production. This phenomenon had attracted many scientists to the problem of elucidating the mechanism of, and reason for, this effect. Several models based on oncogenic studies have been proposed, such as the accumulation of mitochondrial gene mutations, the switch from oxidative phosphorylation respiration to glycolysis, the enhancement of lactate metabolism, and the alteration of glycolytic genes. Whether the Warburg phenomenon is the consequence of genetic dysregulation in cancer or the cause of cancer remains unknown. Moreover, the exact reasons and physiological values of this peculiar metabolism in cancer remain unclear. Although there are some pharmacological compounds, such as 2-deoxy-D-glucose, dichloroacetic acid, and 3-bromopyruvate, therapeutic strategies, including diet, have been developed based on targeting the Warburg effect. In this review, we will revisit the Warburg effect to determine how much scientists currently understand about this phenomenon and how we can treat the cancer based on targeting metabolism.

목차

INTRODUCTION
1. Relationship between tumor-specific glucose metabolism and genetic changes
2. Lactic acid-mediated tumor progression
3. Potential cancer therapy to target the Warburg effects
CONCLUSION AND PERSPECTIVES
REFERENCES

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UCI(KEPA) : I410-ECN-0101-2017-513-000816714