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  • Targeting the SLC7A11/GSH/GPX4 Axis in Cancer: From Redox Homeostasis to Therapeutic Vulnerability

  • Fatemeh Kardooni,1,* Soad Hardani,2
    1. Shahid Chamran University of Ahvaz
    2. Shahid Beheshti University


  • Introduction: Cancer cells continuously adapt their metabolic and redox states to maintain survival under proliferative, oxidative, and therapeutic stress. The SLC7A11/glutathione (GSH)/glutathione peroxidase 4 (GPX4) axis is a central component of this adaptive network, connecting cystine uptake, glutathione synthesis, and lipid peroxide detoxification. Through these functions, the axis contributes to redox homeostasis and membrane integrity and can influence cellular susceptibility to ferroptotic stress and anticancer treatment. Increasing evidence suggests that dysregulation of this pathway may contribute to tumor survival and treatment resistance, although its biological significance is strongly dependent on tumor type and cellular context
  • Methods: Recent mechanistic and preclinical evidence on this axis, ferroptosis, lipid peroxidation, and cancer therapy was reviewed
  • Results: Disruption of SLC7A11/GSH/GPX4 can increase oxidative and lipid stress and may sensitize tumor cells to anticancer treatment. Emerging nanotechnology may improve targeted modulation and drug delivery
  • Conclusion: The SLC7A11/GSH/GPX4 axis represents an important molecular interface linking cystine metabolism, glutathione-dependent antioxidant defense, lipid peroxide control, and ferroptosis susceptibility in cancer. Its therapeutic relevance is likely determined by the broader metabolic and redox landscape of individual tumors rather than by the activity of a single pathway component. Future research should focus on identifying context-specific vulnerabilities, clarifying compensatory resistance mechanisms, and developing rational combination therapies. Integration with advanced nanotechnology-based delivery platforms may further improve the precision and therapeutic window of redox-targeted interventions. A deeper understanding of tumor-specific metabolic dependencies will be essential for translating mechanistic insights into effective and clinically relevant cancer therapies
  • Keywords: SLC7A11; GPX4; Ferroptosis; Cancer; Redox homeostasis

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