Mitochondria-targeted nanoplatforms building for in situ ROS generating photodynamic tumor therapy through reinforcing mitochondria apoptotic pathway

被引:7
|
作者
Wang, Zhiyu [1 ]
Liu, Fengyu [2 ]
Liu, Yuan [3 ]
Huyan, Yucheng [1 ]
Muhammad, Mehdi [1 ]
Xu, Yongqian [1 ]
Li, Hongjuan [1 ]
Sun, Shiguo [1 ,4 ]
机构
[1] Northwest A&F Univ, Coll Chem & Pharm, Shaanxi Key Lab Nat Prod & Chem Biol, Yangling 712100, Shaanxi, Peoples R China
[2] Dalian Univ Technol, Sch Chem, State Key Lab Fine Chem, 2 Linggong Rd, Dalian 116023, Peoples R China
[3] Northwest A&F Univ, Coll Life Sci, Yangling 712100, Shaanxi, Peoples R China
[4] Hebei Univ Sci & Technol, Coll Chem & Pharmaceut Engn, Shijiazhuang 050018, Peoples R China
基金
中国国家自然科学基金;
关键词
Mesoporous silica nanospheres; Mitochondria apoptotic pathway; Photodynamic therapy; Apoptosis inhibitory proteins inhibitors; Photosensitizer; Multimodal cancer treatment; SHOCK-PROTEIN; 90; NANOPARTICLES; INHIBITOR; MECHANISMS;
D O I
10.1016/j.colsurfa.2022.129973
中图分类号
O64 [物理化学(理论化学)、化学物理学];
学科分类号
070304 ; 081704 ;
摘要
Mitochondria-targeted photodynamic therapy (PDT) represents an attractive therapeutic strategy for antitumor therapy. There is growing evidence indicating that in situ generation of reactive oxygen species (ROS) in mitochondria plays a critical role in significant mitochondrial dysfunction and cell apoptosis. Nevertheless, survivin, a member of the inhibitor of apoptosis protein (IAP) family, is overexpressed by PDT stimulation, which inhibit cysteine aspartic acid specific protease-9 (caspase-9) activation and inhibits apoptosis. The corresponding overexpression of Livin protein in tumor cells can inhibit cysteine aspartic acid specific protease-3 (caspase-3) activity, leading to apoptosis inhibition and promoting tumorigenesis and tumor progression. Thus, a precise combination of mitochondria-targeted photodynamic photosensitizers and IAP inhibitor is expected to significantly augment the PDT efficacy. For proof-of-concept, a therapeutic nanoplatform MSNs/GM/I3C-BSA/ MnO2-IR775 (MGIBR) was ingeniously constructed for synergistic cancer therapy. MGIBR can effectively target mitochondria due to the presence of IR775. Under NIR irradiation, MGIBR can generate in situ (1)O(2 )in mitochondria. Importantly, geldanamycin (GM) and indole-3-carbinol (I3C) can inhibit IAP, synergistic enhance PDT and activate mitochondrial apoptosis pathways, leading to effectively cell death. Such a strategy of MGIBR enabled mitochondrial dysfunction based on in situ generation of ROS in mitochondria and IAP inhibitor synergistically, provides a promising paradigm for highly effective cancer therapeutics.
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页数:12
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