摘要
Selectively killing cancer without harming normal tissue is a fundamental challenge in cancer therapy. Elevatedoxidative stress and aberrant redox homeostasis are frequently observed in cancer cells compared with their normalcell counterparts[1]. A small shift toward an oxidizing condition in cells may lead to elevated proliferation andinduction of adaptive response. However, a high oxidizing condition often results in cell injury and cell death.Persistent high level of reactive oxygen species (ROS) in cancer cells usually elicits increased cell proliferation andadaptive responses that may contribute to tumorigenesis, metastasis, and treatment resistance. However, normalcells may still maintain redox homeostasis through adaptive responses. Therefore, regulating intracellular redoxstate may represent an ideal strategy to selectively sensitize cancer cells to oxidative stress-inducing therapy, suchas radiotherapy.
