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Life sciences · Journal article
Acs Nano · November 3, 2026
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Abstract Disruption of the dynamic equilibrium between ferroptotic execution pathways and cellular defense mechanisms can trigger ferroptosis, providing a compelling strategy for tumor suppression and the circumvention of drug resistance. Here, we engineered a Trojan Horse-inspired nanotrap, MIPGPX4@aMOF@CM, that integrates biomimetic recognition, redox-responsive amorphous MOF (aMOF) chemistry, and molecular imprinting to disrupt metal homeostasis and disable key protective pathways, thereby triggering cascade-amplified ferroptosis. The inner core is a molecularly imprinted polymer (MIP) that selectively recognizes GPX4, while the outer shell consists of a novel iron-based aMOF acting as a redox-activated molecular gate and is further cloaked with a cancer cell membrane. This multifunctional nanoplatform enables tumor-specific iron delivery and spatially controlled GPX4 inhibition. Upon homotypic membrane-mediated tumor targeting and cellular internalization, elevated intracellular glutathione (GSH) triggers aMOF degradation, leading to GSH depletion, iron release, and on-demand exposure of the imprinted GPX4 binding sites. This gate-controlled cascade synergistically promotes Fenton chemistry and GPX4 inactivation, substantially disrupting the balance between ferroptotic execution and antioxidant defenses and enhancing tumor-selective ferroptotic responses. Collectively, this work highlights that precisely orchestrating metal homeostasis, redox regulation, and GPX4 inhibition represents a promising strategy for precision ferroptosis-based cancer therapy.