Tumor cell redox and radiosensitization pathways

Tumor cell redox and radiosensitization pathways refer to the integrated network of metabolic and signaling processes that maintain oxidative balance and facilitate DNA repair in cancer cells (PMID: 29107111). These pathways, primarily involving the glutathione (GSH) and thioredoxin (Trx) systems, are frequently upregulated in tumors to mitigate the effects of high metabolic reactive oxygen species (ROS) and provide resistance to ionizing radiation (PMID: 25653113). Radiosensitization is achieved by pharmacologically targeting these systems—for instance, using buthionine sulfoximine (BSO) to deplete GSH or auranofin to inhibit thioredoxin reductase—thereby increasing the susceptibility of tumor cells to radiation-induced oxidative damage (PMID: 15574350, PMID: 28651543). Furthermore, inhibiting the Nrf2-mediated antioxidant response or DNA repair enzymes like PARP can synergistically enhance the efficacy of radiotherapy (PMID: 30605714, PMID: 24631615). Despite their potential, the clinical utility of targeting these pathways is often limited by the need to maintain a therapeutic window that spares normal tissues from excessive oxidative injury.

Other names

Redox homeostasis pathwaysOxidative stress responseRadiosensitization signalingAntioxidant defense pathways

Inhibition of antioxidant defense systems and DNA repair mechanisms to increase intracellular reactive oxygen species and enhance radiation-induced cell death.