부산대학교 도서관

Metabolic alterations and elevated levels of reactive oxygen species (ROS) are two characteristics of cancer. The metabolic patterns of cancer cells are elaborately reprogrammed to fulfill the high biomass demands of rapid propagation. ROS, the byproducts of metabolic processes, are accumulated in cancer cells partially due to metabolic abnormalities or oncogenic mutations. To prevent oxidative damage, cancer cells can orchestrate metabolic adaptation to maintain reduction–oxidation (redox) balance by producing reducing equivalents. ROS, acting as second messengers, can in turn manipulate metabolic pathways by directly or indirectly affecting the function of metabolic enzymes. In this review we discuss how cancer cell metabolism and redox signaling are intertwined, with an emphasis on the perspective of targeting metabolic–redox circuits for cancer therapy. Highlights Metabolic reprogramming and oxidative stress are major characteristics of cancer; targeting of metabolic or redox vulnerabilities appears to hold promise for cancer therapy. Cancer cell metabolism and redox signaling are intimately coupled, dynamically constituting intrinsic metabolic–redox circuits that facilitate cell growth and proliferation. Brisk metabolic or redox adaptation occurs when cancer cells are subjected to metabolism- or ROS-targeted therapy, contributing to compromised outcome or drug resistance. ROS, acting as second messengers, could induce direct oxidative modifications on the active cysteine residues of metabolic enzymes, leading to functional changes of metabolic enzymes and subsequent metabolic switches. [ABSTRACT FROM AUTHOR]