Open AccessUltrathin‐FeOOH‐Coated MnO 2 Sonosensitizers with Boosted Reactive Oxygen Species Yield and Remodeled Tumor Microenvironment for Efficient Cancer Therapy
Author(s) -
Liu Qiyu,
Shi Liyin,
Liao Ying,
Cao Xianshuo,
Liu Xiaoqing,
Yu Yanxia,
Wang Zifan,
Lu Xihong,
Wang Jianwei
Publication year - 2022
Publication title -
advanced science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.388
H-Index - 100
ISSN - 2198-3844
DOI - 10.1002/advs.202200005
Subject(s) - reactive oxygen species , sonodynamic therapy , tumor microenvironment , chemistry , catalase , singlet oxygen , glutathione , tumor hypoxia , cancer research , oxygen , hydroxyl radical , mitochondrial ros , hypoxia (environmental) , in vivo , radical , biophysics , glutathione peroxidase , superoxide , oxidative stress , biochemistry , medicine , radiation therapy , biology , tumor cells , organic chemistry , surgery , microbiology and biotechnology , enzyme
Sonodynamic therapy (SDT) typically suffers from compromised anticancer efficacy owing to the low reactive oxygen species (ROS) yield and complicated tumor microenvironment (TME) which can consume ROS and support the occurrence and development of tumors. Herein, ultrathin‐FeOOH‐coated MnO 2 nanospheres (denoted as MO@FHO) as sonosensitizers which can not only facilitate ultrasound (US)‐triggered ROS but also tune the TME by hypoxia alleviation, H 2 O 2 consumption as well as glutathione (GSH) depletion are designed. The FeOOH coating will boost the production yield of singlet oxygen ( 1 O 2 ) and hydroxyl radicals ( • OH) by inhibiting the recombination of US‐initiated electron–hole pairs and Fenton‐like reaction, respectively. Additionally, the catalase‐like and GSH peroxidase‐like activities of MO@FHO nanospheres enable them to break the TME equilibrium via hypoxia alleviation and GSH depletion. The combination of high ROS yield and fundamental destruction of TME equilibrium results in satisfactory antitumor outcomes, as demonstrated by the high tumor suppression efficacy of MO@FHO on MDA‐MB‐231‐tumor‐bearing mice. No obvious toxicity is detected to normal tissues at therapeutic doses in vivo. The capability to modulate the ROS production and TME simultaneously can afford new probability for the development of advanced sonosensitizers for synergistic comprehensive cancer therapy.