中国科学院机构知识库网格
Chinese Academy of Sciences Institutional Repositories Grid
首页 机构 成果 学者
  
  1. CAS IR Grid
  2. 合肥物质科学研究院
  3. 中国科学院合肥物质科学研究院
Rationally designed catalytic nanoplatform for enhanced chemoimmunotherapy via deploying endogenous plus exogenous copper and remodeling tumor microenvironment

文献类型：期刊论文

作者Sun, Daxi1; Yu, Liting1; Wang, Gang2; Xu, Yuxue1; Wang, Peng1; Wang, Ningning1; Wu, Zhengyan3,4; Zhang, Guilong1; Zhang, Jia3,4; Zhang, Yunjiao5
刊名JOURNAL OF NANOBIOTECHNOLOGY
出版日期2024-09-09
卷号22
关键词Copper peroxide Chemodynamic therapy Chloroquine Autophagy Immunogenic cell death, MHC-II
DOI10.1186/s12951-024-02696-x
通讯作者Wu, Zhengyan(zywu@ipp.ac.cn) ; Tian, Geng(tiangeng@bzmc.edu.cn) ; Wei, Pengfei(pfwei@bzmc.edu.cn)
英文摘要Chemodynamic therapy represents a novel tumor therapeutic modality via triggering catalytic reactions in tumors to yield highly toxic reactive oxygen species (ROS). Nevertheless, low efficiency catalytic ability, potential systemic toxicity and inefficient tumor targeting, have hindered the efficacy of chemodynamic therapy. Herein, a rationally designed catalytic nanoplatform, composed of folate acid conjugated liposomes loaded with copper peroxide (CP) and chloroquine (CQ; a clinical drug) (denoted as CC@LPF), could power maximal tumor cytotoxicity, mechanistically via maneuvering endogenous and exogenous copper for a highly efficient catalytic reaction. Despite a massive autophagosome accumulation elicited by CP-powered autophagic initiation and CQ-induced autolysosomal blockage, the robust ROS, but not aberrant autophagy, underlies the synergistic tumor inhibition. Otherwise, this combined mode also elicits an early onset, above all, long-term high-level existence of immunogenic cell death markers, associated with ROS and aberrant autophagy -triggered endoplasmic reticulum stress. Besides, CC@LPF, with tumor targeting capability and selective tumor cytotoxicity, could elicit intratumor dendritic cells (mainly attributed to CQ) and tumor infiltrating CD8+ T cells, upon combining with PD-L1 therapeutic antibody, further induce significant anti-tumor effect. Collectively, the rationally designed nanoplatform, CC@LPF, could enhance tumor chemoimmunotherapy via deploying endogenous plus exogenous copper and remodeling tumor microenvironment.
WOS关键词CELL-DEATH ; AUTOPHAGY ; CANCER ; INHIBITION ; TOXICITY ; ACTIVATION ; STRESS ; H2O2
资助项目Yantai Science and Technology Innovation Development Plan Project
WOS研究方向Biotechnology & Applied Microbiology ; Science & Technology - Other Topics
语种英语
WOS记录号WOS:001308654100001
出版者BMC
资助机构Yantai Science and Technology Innovation Development Plan Project
源URL[http://ir.hfcas.ac.cn:8080/handle/334002/135203]  
专题中国科学院合肥物质科学研究院
通讯作者Wu, Zhengyan; Tian, Geng; Wei, Pengfei
作者单位1.Binzhou Med Univ, Shandong Technol Innovat Ctr Mol Targeting & Intel, Sch Pharm, Yantai 264003, Peoples R China
2.Soochow Univ, Inst Funct Nano & Soft Mat FUNSOM, Jiangsu Key Lab Carbon Based Funct Mat & Devices, Suzhou 215123, Peoples R China
3.Chinese Acad Sci, Hefei Inst Phys Sci, Key Lab High Magnet Field & Ion Beam Phys Biol, Hefei 230031, Peoples R China
4.Univ Sci & Technol China, Hefei 230026, Peoples R China
5.South China Univ Technol, Affiliated Hosp 2, Sch Med, Guangzhou 510006, Peoples R China
推荐引用方式
GB/T 7714		 Sun, Daxi,Yu, Liting,Wang, Gang,et al. Rationally designed catalytic nanoplatform for enhanced chemoimmunotherapy via deploying endogenous plus exogenous copper and remodeling tumor microenvironment[J]. JOURNAL OF NANOBIOTECHNOLOGY,2024,22.
APA Sun, Daxi.,Yu, Liting.,Wang, Gang.,Xu, Yuxue.,Wang, Peng.,...&Wei, Pengfei.(2024).Rationally designed catalytic nanoplatform for enhanced chemoimmunotherapy via deploying endogenous plus exogenous copper and remodeling tumor microenvironment.JOURNAL OF NANOBIOTECHNOLOGY,22.
MLA Sun, Daxi,et al."Rationally designed catalytic nanoplatform for enhanced chemoimmunotherapy via deploying endogenous plus exogenous copper and remodeling tumor microenvironment".JOURNAL OF NANOBIOTECHNOLOGY 22(2024).

入库方式： OAI收割

来源：合肥物质科学研究院

浏览0
下载0
收藏0
其他版本

除非特别说明，本系统中所有内容都受版权保护，并保留所有权利。