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The cancer cell redox system and glycolytic machinery refer to the integrated metabolic and antioxidant pathways that support the rapid proliferation and survival of malignant cells. Cancer cells frequently exhibit the Warburg effect, characterized by increased glucose uptake and lactic acid fermentation even in the presence of oxygen, which provides necessary building blocks for biomass (Warburg, 1956). To survive the resulting increase in metabolic byproducts and reactive oxygen species (ROS), these cells upregulate antioxidant systems such as the glutathione and thioredoxin pathways (Gorrini et al., 2013). Therapeutic strategies targeting this system aim to create a "metabolic catastrophe" by inhibiting glucose uptake or processing while concurrently disabling the cell's ability to manage oxidative stress (Pelicano et al., 2006). This dual approach is designed to selectively induce apoptosis in cancer cells, which are more dependent on these pathways than healthy cells (Trachootham et al., 2009). Interacting drugs like 2-deoxy-D-glucose and imexon work by disrupting these specific metabolic vulnerabilities. However, because these processes are fundamental to cellular life, achieving selectivity remains a significant challenge in drug development.
Simultaneous inhibition of glycolytic flux and depletion of antioxidant capacity to induce oxidative-stress-mediated cell death.
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