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Therapeutically, disulfidptosis exploits metabolic vulnerabilities in SLC7A11-high tumors: while SLC7A11 confers resistance to ferroptosis/apoptosis, its overexpression creates glucose dependency, rendering cells susceptible to GLUT inhibitors—as demonstrated in KEAP1-mutant lung cancers where SLC7A11 upregulation drives disulfide accumulation under glucose starvation (Xiao et al., 2024)
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