Abstract
Redox homeostasis is not only essential for the maintenance of normal physiological functions, but also plays an important role in the growth, survival, and therapy resistance of cancer cells. Altered redox balance and consequent disruption of redox signaling are implicated in the proliferation and progression of cancer cells and their resistance to chemo- and radiotherapy. The nuclear factor erythroid 2 p45-related factor (Nrf2) is the principal stress-responsive transcription factor that plays a pivotal role in maintaining cellular redox homeostasis. Aberrant Nrf2 overactivation has been observed in many cancerous and transformed cells. Uncontrolled amplification of Nrf2-mediated antioxidant signaling results in reductive stress. Some metabolic pathways altered due to reductive stress have been identified as major contributors to tumorigenesis. This review highlights the multifaceted role of reductive stress in cancer development and progression.
Highlights
Cellular redox homeostasis is essential for proper transmission of the intracellular signaling involved in normal physiological processes
Treatment with antioxidants was found to promote the survival of cells through into metabolic reactions catalyzed by the malic enzyme (ME) and isocitrate dehydrogenase 1 (IDH1)
IDH ablation diminished nicotinamide adenine dinucleotide phosphate (NADPH) levels in transformed glioma cells and, when combined with a receptor tyrosine kinase inhibitor cocktail, caused a reduction in GSH with a concomitant increase in reactive oxygen species (ROS) and apoptosis [74]. These findings suggest that IDH1 upregulation represents a common metabolic adaptation of cancer cells to support macromolecular synthesis, aggressive growth, and therapeutic resistance
Summary
Cellular redox homeostasis is essential for proper transmission of the intracellular signaling involved in normal physiological processes. Reductive stress is likely to be derived from intrinsic signals that enable cellular defense against pro-oxidative conditions It is triggered by alterations in the. It is triggered by alterations production and/or utilization of reducing equivalents. It is noteworthy of ROS, this can eventually facilitate the development of drug resistance It is notethat a reductive redox environment fosters cancer and metastasis [11].
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