Atovaquone-induced oxidative stress activates the pentose phosphate pathway and Immunogenic cell death in ovarian cancer
8.5
来源：
Nature
关键字：
de novo drug design
发布时间：
2025-11-25 08:11
摘要：
Atovaquone, an FDA-approved oxidative phosphorylation inhibitor, shows promise in treating epithelial ovarian cancer (EOC) by inducing oxidative stress and activating immune responses. The study reveals that atovaquone disrupts cellular metabolism, activates the pentose phosphate pathway, and enhances immunogenic cell death, making EOC cells more susceptible to treatment. Notably, atovaquone increases the expression of damage-associated molecular patterns (DAMPs) and enhances natural killer (NK) cell activity, suggesting its potential as a combination therapy in EOC treatment. These findings pave the way for further exploration of atovaquone in cancer therapy.
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关键证据
Atovaquone induces oxidative stress and activates immune recognition in EOC cells.
The study reveals significant changes in gene expression related to redox homeostasis and immune activation.
Atovaquone enhances NK cell activity, suggesting its potential in immunotherapy.
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AI评分总结
Atovaquone, an FDA-approved oxidative phosphorylation inhibitor, shows promise in treating epithelial ovarian cancer (EOC) by inducing oxidative stress and activating immune responses. The study reveals that atovaquone disrupts cellular metabolism, activates the pentose phosphate pathway, and enhances immunogenic cell death, making EOC cells more susceptible to treatment. Notably, atovaquone increases the expression of damage-associated molecular patterns (DAMPs) and enhances natural killer (NK) cell activity, suggesting its potential as a combination therapy in EOC treatment. These findings pave the way for further exploration of atovaquone in cancer therapy.