2. Academic Validation
  3. Photodynamic Therapy Initiated Ferrotherapy of Self-Delivery Nanomedicine to Amplify Lipid Peroxidation via GPX4 Inactivation

Photodynamic Therapy Initiated Ferrotherapy of Self-Delivery Nanomedicine to Amplify Lipid Peroxidation via GPX4 Inactivation

  • ACS Appl Mater Interfaces. 2022 Nov 18. doi: 10.1021/acsami.2c15495.
Lin-Ping Zhao 1 2,  Shao-Yi Chen 1,  Rong-Rong Zheng 1,  Xiao-Na Rao 1,  Ren-Jiang Kong 3,  Chu-Yu Huang 1,  Yi-Bin Liu 4,  Youzhi Tang 4,  Hong Cheng 3,  Shi-Ying Li 1
Affiliations

Affiliations

  • 1 Guangdong Provincial Key Laboratory of Molecular Target & Clinical Pharmacology, the NMPA and State Key Laboratory of Respiratory Disease, School of Pharmaceutical Sciences and the Fifth Affiliated Hospital, Guangzhou Medical University, Guangzhou 511436, China.
  • 2 Key Laboratory of Biological Targeting Diagnosis, Therapy and Rehabilitation of Guangdong Higher Education Institutes, The Fifth Affiliated Hospital of Guangzhou Medical University, Guangzhou 510700, China.
  • 3 Biomaterials Research Center, School of Biomedical Engineering, Southern Medical University, Guangzhou 510515, China.
  • 4 Guangdong Provincial Key Laboratory of Veterinary Pharmaceutics Development and Safety Evaluation, College of Veterinary Medicine, South China Agricultural University, Guangzhou 510642, China.
PMID: 36399048 DOI: 10.1021/acsami.2c15495
Abstract

Lipid peroxide (LPO) is the hallmark of Ferroptosis, which is a promising antitumor modality for its unique advantages. However, a cellular defense system would weaken the antitumor efficacy of ferrotherapy. Herein, a GPX4 inhibitor of ML162 and a photosensitizer of chlorine e6 (Ce6) are used to prepare the self-delivery nanomedicine (C-ML162) through hydrophobic and electrostatic interactions to enhance Ferroptosis by photodynamic therapy (PDT). Specifically, carrier-free C-ML162 improves the solubility, stability, and cellular uptake of antitumor agents. Upon LIGHT irradiation, the internalized C-ML162 generates large amounts of Reactive Oxygen Species (ROS) to oxidize cellular unsaturated lipid into LPO. More importantly, C-ML162 can directly inactivate GPX4 to enhance the accumulation of toxic LPO, inducing ferroptotic cell death. Additionally, C-ML162 is capable of accumulating at a tumor site for effective treatment. This self-delivery system to amplify lipid peroxidation via GPX4 inactivation for PDT initiated ferrotherapy might provide an appealing strategy against malignancies.

Keywords

GPX4 inactivation; carrier free; ferrotherapy; lipid peroxides; photodynamic therapy.

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