A Functional Nanocomposite Tri‐Activates Cuproptosis, Ferroptosis, and Mitophagy Death Pathway to Oppose Malignancies

A copper-based nanoplatform demonstrates potent tumor suppression across multiple models.

• The engineered nanoplatform, Cu-MOF@DPCPX, targets multiple metal-dependent death pathways in cancer cells.
• Copper overload in tumors triggers cuproptosis by promoting protein aggregation and loss of iron-sulfur clusters.
• Copper-induced reactions generate hydroxyl radicals and reduce protective enzymes, leading to ferroptosis.
• Mitochondrial damage from these processes activates mitophagy, further amplifying cell death through copper release.
• In vivo results indicate increased infiltration of CD8⁺ T-cells and polarization of M1 macrophages in tumor microenvironments.

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