ROS and energy metabolism in cancer cells: Alliance for fast growth

Sang Won Kang, Sunmi Lee, Eun Kyung Lee

Research output: Contribution to journalReview articlepeer-review

64 Scopus citations

Abstract

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.

Original languageEnglish
Pages (from-to)338-345
Number of pages8
JournalArchives of Pharmacal Research
Volume38
Issue number3
DOIs
StatePublished - Mar 2015

Keywords

  • Antioxidant enzyme
  • Energy metabolism
  • NADPH oxidase
  • Reactive oxygen species

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