Redox balance in cancer cells

Cancer cells exhibit a unique redox balance characterized by elevated ROS production due to increased metabolic activity and oncogenic signaling. To survive and proliferate, they upregulate antioxidant systems (glutathione, thioredoxin, peroxiredoxins, and related enzymes) and metabolic pathways (pentose phosphate pathway, glutaminolysis) to neutralize excess ROS. This tight regulation allows tumors to use ROS for signal transduction and metabolic reprogramming while preventing lethal oxidative damage. The redox adaptability of cancer cells underpins their resistance to chemotherapy, radiotherapy, and oxidative stress-induced cell death, making redox homeostasis and its constituent molecules attractive therapeutic targets. However, "redox balance" itself is not a molecule or receptor but a collection of processes; actionable targets often include individual enzymes (e.g., glutathione peroxidase), transporters (e.g., xCT), or transcription factors (e.g., NRF2). For precise targeting or structured database curation, specify individual molecular targets (such as NRF2, Glutathione, Thioredoxin, etc.) rather than the broad "redox balance in cancer cells."

Other names

redox homeostasis in cancerredox regulation in cancercellular redox balanceoxidative stress balance in tumor cells

Inhibition of antioxidant systems (increasing ROS beyond the cancer cell's tolerance, leading to cell death); Modulation of redox-sensitive metabolic pathways; Induction of oxidative stress; Disruption of glutathione or thioredoxin systems.