Triggering Reactive Oxygen Species Field Effect Transistor Based on HIF‐1α Signaling for Enhanced Chemodynamic Therapy

Abstract A hypoxic tumor microenvironment (TME) makes tumors resistant to various therapies including chemotherapies, radiotherapies, and photodynamic therapies. Here, a new strategy of building a reactive oxygen species (ROS) field effect transistor (FET) is reported, which enables amplified ROS flux for tumor ablation and addresses the challenge of tumor hypoxia by a liposomal delivery system (SN‐38∩LP@Fe 3 O 4 /GOx). This design can switch “ON” the ROS FET by a small tuning on the “gate electrode” with downregulation of HIF‐1α signaling. Highly effective tumor ablation both in vitro and in vivo using the ROS FET strategy is demonstrated, and its mechanism of changing tumor hypoxia is revealed. Distinctly different from the previous reports based on the chemical supply to address hypoxia TME, this work conceptually creates a method of maximizing ROS damages for cancer treatment with well‐leveraged modulation of the tumor hypoxia pathways.