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An iron logic unites bacterial and cancer persister cells
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DOI：10.1038/s41580-026-01010-x.png)
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Abstract
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Mirroring bacterial persisters, cancer cells reprogram their iron homeostasis to acquire a drug-tolerant cell state that paradoxically confers vulnerability to ferroptosis. We propose a conserved principle, positioning iron as a driver of cell adaptations across mammalian malignant and microbial persistence. Bacterial persisters and drug-tolerant persister cells in cancer both show reprogrammed iron homeostasis and a vulnerability to ferroptosis. Agostinis and Rodriguez propose that this iron logic is a conserved principle with implications for therapeutics development.
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