ROS and energy metabolism in cancer cells: alliance for fast growth.

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.