Defect self-assembly of metal-organic framework triggers ferroptosis to overcome resistance

被引:92
作者
Peng, Haibao [1 ,2 ,3 ]
Zhang, Xingcai [5 ]
Yang, Peng [6 ]
Zhao, Jiaxu [1 ]
Zhang, Wei [1 ]
Feng, Nianping [3 ]
Yang, Wuli [2 ]
Tang, Jing [4 ]
机构
[1] Fudan Univ, Inst Translat Brain Res, Shanghai 200032, Peoples R China
[2] Fudan Univ, Dept Macromol Sci, State Key Lab Mol Engn Polymers, Shanghai 200438, Peoples R China
[3] Shanghai Univ Tradit Chinese Med, Dept Pharmaceut Sci, Shanghai 201203, Peoples R China
[4] Stanford Univ, Dept Mat Sci & Engn, Stanford, CA 94305 USA
[5] MIT, Sch Engn, Cambridge, MA 02139 USA
[6] Xidian Univ, Engn Res Ctr Mol & Neuro Imaging Minist Educ, Sch Life Sci & Technol, Xian 710126, Peoples R China
基金
上海市自然科学基金; 中国国家自然科学基金; 中国博士后科学基金;
关键词
Metal-organic framework; Defect nanostructures; Ferroptosis; Membrane-camouflaged; Multi-drug-delivery; ONE-POT SYNTHESIS; MULTIDRUG-RESISTANCE; APOPTOSIS;
D O I
10.1016/j.bioactmat.2021.12.018
中图分类号
R318 [生物医学工程];
学科分类号
0831 ;
摘要
The emergence of multidrug treatment resistance presents a hurdle for the successful chemotherapy of tumours. Ferroptosis, resulting from the iron-dependent accumulation of lipid peroxides, has the potential to reverse multidrug resistance. However, simultaneous delivery of the iron sources, ferroptosis inducers, drugs, and enhanced circulation carriers within matrices remains a significant challenge. Herein, we designed and fabricated a defect self-assembly of metal-organic framework (MOF)-red blood cell (RBC) membrane-camouflaged multi-drug-delivery nanoplatform for combined ferroptosis-apoptosis treatment of multidrug-resistant cancer. Ferroptosis and chemotherapeutic drugs are embedded in the centre of the iron (III)-based MOF at defect sites by coordination with metal clusters during a one-pot solvothermal synthesis process. The RBC membrane could camouflage the nanoplatform for longer circulation. Our results demonstrate that this defect self-assemblyenabled MOF-membrane-camouflaged nanoplatform could deplete the glutathione, amplify the reactive oxidative species oxidative stress, and enable remarkable anticancer properties. Our work provides an alternative strategy for overcoming multidrug resistance, which could regulate the fluidity and permeability of the cell membrane by ferroptosis to downregulate of P-glycoprotein protein expression by ferroptosis. This defect selfassembly-enabled MOF-membrane-camouflaged multi-drug-delivery nanoplatform has great therapeutic potential.
引用
收藏
页码:1 / 11
页数:11
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