Demonstrates improved therapeutic outcomes in hepatocellular carcinoma by targeting ATOX1-mediated copper homeostasis, suggesting a novel approach.
Copper metabolism dysregulation is a defining feature of TACE-refractory HCC. Targeting ATOX1-mediated copper homeostasis using Cu²⁺/DC_AC50@PNA represents a novel and effective strategy to induce cuproptosis, overcome TACE refractoriness, and improve therapeutic outcomes in HCC.
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