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Redox Dyshomeostasis with Dual Stimuli-Activatable Dihydroartemisinin Nanoparticles to Potentiate Ferroptotic Therapy of Pancreatic Cancer

文献类型：期刊论文

作者Wang, Yingjie1,2; Chen, Fangmin2,3; Zhou, Huiling2; Huang, Lujia2; Ye, Jiayi2; Liu, Xiaoying2; Sheng, Weizhong4; Gao, Weidong4; Yu, Haijun2,3; Wang, Feng1
刊名SMALL METHODS
出版日期2022-11-29
页码13
ISSN号2366-9608
关键词combinatory therapy dual stimuli-responsive ferroptosis immunotherapy pancreatic cancer
DOI10.1002/smtd.202200888
通讯作者Sheng, Weizhong(Sheng.weizhong@zs-hospital.sh.cn) ; Yu, Haijun(hjyu@simm.ac.cn) ; Wang, Feng(prof.fengwang@tongji.edu.cn)
英文摘要Pancreatic ductal adenocarcinoma (PDAC) is highly lethal and resistant to conventional therapies, including chemo-, radio-, and immunotherapy. In this study, it is first determined that a combination of dihydroartemisinin (DHA) and RSL-3 (a glutathione peroxidase 4 (GPX4) inhibitor) markedly induced ferroptosis of PDAC tumor cells. A mechanistic study revealed that DHA can react with iron ions to generate carbon radicals and deplete intracellular glutathione, thereby cumulatively triggering the lipid peroxidation of tumor cells with RSL-3-mediated GPX4 inhibition. A DHA-conjugated amphiphilic copolymer is subsequently synthesized, and intracellular acidity and oxidation dual-responsive DHA nanoparticles are further engineered for the tumor-specific co-delivery of DHA and RSL-3. The resultant nanoparticles (PDBA@RSL-3) efficiently induce ferroptosis of tumor cells in the Panc02 tumor-bearing immune-deficient mouse model, and elicit T-cell-based antitumor immunity in the immune-competent mouse model. The combination of PDBA@RSL-3 nanoparticles and programmed death ligand 1 blockade therapy efficiently inhibits PDAC tumor growth in the immune-competent mouse models. This study may provide novel insights for treatment of PDAC with ferroptosis-based immunotherapy.
WOS关键词CELL-DEATH ; BLOCKADE ; PD-L1 ; IRON
资助项目National Natural Science Foundation of China[81972287] ; National Natural Science Foundation of China[51873228] ; Science and Technology Commission of Shanghai Municipality[20430711800] ; Science and Technology Commission of Shanghai Municipality[19ZR1447600] ; Open Funds of State Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, CAS[SIMM2105KF-12]
WOS研究方向Chemistry ; Science & Technology - Other Topics ; Materials Science
语种英语
出版者WILEY-V C H VERLAG GMBH
WOS记录号WOS:000891943800001
源URL[http://119.78.100.183/handle/2S10ELR8/304303]  
专题中国科学院上海药物研究所
通讯作者Sheng, Weizhong; Yu, Haijun; Wang, Feng
作者单位1.Fudan Univ, Huadong Hosp, Shanghai Med Coll, Dept Gastroenterol, Shanghai 200040, Peoples R China
2.Chinese Acad Sci, Shanghai Inst Mat Med, Ctr Pharmaceut, Shanghai 201203, Peoples R China
3.Univ Chinese Acad Sci, Beijing 100049, Peoples R China
4.Fudan Univ, Zhongshan Hosp, Dept Gen Surg, Shanghai 200032, Peoples R China
推荐引用方式
GB/T 7714		 Wang, Yingjie,Chen, Fangmin,Zhou, Huiling,et al. Redox Dyshomeostasis with Dual Stimuli-Activatable Dihydroartemisinin Nanoparticles to Potentiate Ferroptotic Therapy of Pancreatic Cancer[J]. SMALL METHODS,2022:13.
APA Wang, Yingjie.,Chen, Fangmin.,Zhou, Huiling.,Huang, Lujia.,Ye, Jiayi.,...&Wang, Feng.(2022).Redox Dyshomeostasis with Dual Stimuli-Activatable Dihydroartemisinin Nanoparticles to Potentiate Ferroptotic Therapy of Pancreatic Cancer.SMALL METHODS,13.
MLA Wang, Yingjie,et al."Redox Dyshomeostasis with Dual Stimuli-Activatable Dihydroartemisinin Nanoparticles to Potentiate Ferroptotic Therapy of Pancreatic Cancer".SMALL METHODS (2022):13.

入库方式： OAI收割

来源：上海药物研究所

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