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The mechanism

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second, cisplatin can directly inhibit the physiological function of human iron regulatory protein 2 by covalently binding to its cysteine residue sites (Cys512 and Cys516), disrupting the homeostasis of systemic iron metabolism, causing persistent intracellular iron deficiency, and further aggravating refractory anemia (Miyazawa et al

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Due to its reduced affinity for IGF-binding proteins, IGF-1 LR3 may remain bioavailable in experimental settings, potentially influencing cellular responses over extended periods