ROS and energy metabolism in cancer cells: alliance for fast growth
- 주제(키워드) Antioxidant enzyme , Energy metabolism , NADPH oxidase , Reactive oxygen species
- 등재 SCIE, KCI등재, SCOPUS
- 발행기관 Pharmaceutical Society of Korea
- 발행년도 2015
- 총서유형 Journal
- URI http://www.dcollection.net/handler/ewha/000000114244
- 본문언어 영어
- Published As http://dx.doi.org/10.1007/s12272-015-0550-6
- 저작권 이화여자대학교 논문은 저작권에 의해 보호받습니다.
초록/요약
In normal cells, the cellular reactive oxygen species (ROS) level is proportional to the activity of mitochondrial electron transport and tightly controlled by endogenous antioxidant system. However, energy metabolism and ROS homeostasis in cancer cells are much different from those in normal cells. For example, a majority of cellular glucose is metabolized through aerobic glycolysis (“Warburg effect”) and the pentose phosphate pathway. Cancer cells harbor functional mitochondria, but many mutations in nuclear DNA-encoded mitochondrial genes and mitochondrial genome result in the mitochondrial metabolic reprogramming. The other characteristic of cancer cells is to maintain much higher ROS level than normal cells. Ironically, cancer cells overexpress the ROS-producing NADPH oxidase and the ROS-eliminating antioxidant enzymes, both of which enzyme systems share NADPH as a reducing power source. In this article, we review the complex connection between ROS and energy metabolisms in cancer cells.
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