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Bimetallic Oxide FeWO X Nanosheets as Multifunctional Cascade Bioreactors for Tumor Microenvironment‐Modulation and Enhanced Multimodal Cancer Therapy
Author(s) -
Gong Fei,
Chen Muchao,
Yang Nailin,
Dong Ziliang,
Tian Longlong,
Hao Yu,
Zhuo Mingpeng,
Liu Zhuang,
Chen Qian,
Cheng Liang
Publication year - 2020
Publication title -
advanced functional materials
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.069
H-Index - 322
eISSN - 1616-3028
pISSN - 1616-301X
DOI - 10.1002/adfm.202002753
Subject(s) - tumor microenvironment , materials science , reactive oxygen species , cytotoxic t cell , oxidative stress , glutathione , cancer immunotherapy , cancer cell , immune system , cancer research , biophysics , hydrogen peroxide , immunotherapy , chemistry , cancer , biochemistry , biology , immunology , enzyme , genetics , in vitro
Modulating the hostile tumor microenvironment (TME) rather than directly killing cancer cells may be an effective strategy to improve the therapeutic benefits in cancer treatment. Herein, FeWO X nanosheets are constructed as cascade bioreactors to modulate the TME and enhance radiotherapy and immunotherapy of tumors. Synthesized by the thermal‐decomposition method and modified by poly(ethylene glycol) (PEG), the obtained FeWO X ‐PEG with multivalent metal elements (Fe 2+/3+ , W 5+/6+ ) exhibit efficient catalytic decomposition of hydrogen peroxide (H 2 O 2 ) to generate hydroxyl radicals (•OH) for chemo‐dynamic therapy (CDT). The generated high valence of metal ions (Fe 3+ /W 6+ ) in FeWO X ‐PEG are reduced by endogenous glutathione (GSH), both leading to depletion of GSH and further amplified oxidative stress, and resulting in the reduced metal valence statuses (Fe 2+ /W 5+ ) enabling cascade bioreactions. Such FeWO X ‐PEG bioreactors enhance the oxidative stress in the tumor and interact with X‐rays, significantly improving cancer radiotherapy (RT). Furthermore, the reactive oxygen species (ROS)‐induced inflammation caused by FeWO X ‐PEG in TME activates the immune system and promotes the tumor‐infiltration of various types of immune cells, which working together with cytotoxic T‐lymphocyte antigen‐4 (CTLA‐4) checkpoint blockade could elicits a robust immune response to defeat tumors.