中国科学院机构知识库网格
Chinese Academy of Sciences Institutional Repositories Grid
Caspase-3-mediated GSDME induced Pyroptosis in breast cancer cells through the ROS/JNK signalling pathway

文献类型:期刊论文

作者Zhang, Ziwen1,2,3; Zhang, Han2; Li, Dongbo2; Zhou, Xiaoping2; Qin, Qi2; Zhang, Qingyuan2
刊名JOURNAL OF CELLULAR AND MOLECULAR MEDICINE
出版日期2021-08-08
ISSN号1582-1838
关键词breast cancer doxorubicin GSDME pyroptosis ROS JNK pathway
DOI10.1111/jcmm.16574
通讯作者Zhang, Qingyuan(zzw2044@21cn.com)
英文摘要Pyroptosis is a new form of programmed cell death generated by some inflammasomes, piloting the cleavage of gasdermin (GSDM) and stimulation of dormant cytokines like IL-18 and IL-1 beta; these reactions are narrowly linked to certain diseases like diabetic nephropathy and atherosclerosis. Doxorubicin, a typical anthracycline, and famous anticancer drug has emerged as a prominent medication in several cancer chemotherapies, although its application is accompanied with expending of dose-dependent, increasing, irreversible and continuing cardiotoxic side effects. However, the exact path that links the induced pyroptosis to the mechanism by which Doxorubicin (DOX) acts against breast cancer cells is still puzzling. The present study seeks to elucidate the potential link between DOX-induced cell death and pyroptosis in two human breast cancer cell lines (MDA-MB-231 and T47D). We proved that treatment with DOX reduced the cell viability in a dose-dependent way and induced pyroptosis morphology in MDA-MB-231 and T47D cells. Also, protein expression analyses revealed GSDME as a key regulator in DOX-induced pyroptosis and highlighted the related role of Caspase-3 activation. Furthermore, DOX treatments induced intracellular accumulation of ROS, stimulated the phosphorylation of JNK, and Caspase-3 activation, subsequently. In conclusion, the study suggests that GSDME triggered DOX-induced pyroptosis in the caspase-3 dependent reactions through the ROS/JNK signalling pathway. Additionally, it showed that the DOX-induced cardiotoxicity and pyroptosis in breast cancer cells can be minimized by reducing the protein level of GSDME; thus, these outcomes provide a new research target and implications for the anticancer investigations and therapeutic applications.
WOS关键词DOXORUBICIN ; MANAGEMENT ; CLEAVAGE
资助项目National Natural Science Foundation of China[81730074] ; National Natural Science Foundation of China[81672599]
WOS研究方向Cell Biology ; Research & Experimental Medicine
语种英语
出版者WILEY
WOS记录号WOS:000682934100001
资助机构National Natural Science Foundation of China
源URL[http://ir.hfcas.ac.cn:8080/handle/334002/124251]  
专题中国科学院合肥物质科学研究院
通讯作者Zhang, Qingyuan
作者单位1.Chinese Acad Sci, Inst Canc & Basic Med IBMC, Hangzhou, Peoples R China
2.Harbin Med Univ, Canc Hosp, Dept Med Oncol, Harbin 150081, Peoples R China
3.Univ Chinese Acad Sci, Zhejiang Canc Hosp, Canc Hosp, Hangzhou, Peoples R China
推荐引用方式
GB/T 7714
Zhang, Ziwen,Zhang, Han,Li, Dongbo,et al. Caspase-3-mediated GSDME induced Pyroptosis in breast cancer cells through the ROS/JNK signalling pathway[J]. JOURNAL OF CELLULAR AND MOLECULAR MEDICINE,2021.
APA Zhang, Ziwen,Zhang, Han,Li, Dongbo,Zhou, Xiaoping,Qin, Qi,&Zhang, Qingyuan.(2021).Caspase-3-mediated GSDME induced Pyroptosis in breast cancer cells through the ROS/JNK signalling pathway.JOURNAL OF CELLULAR AND MOLECULAR MEDICINE.
MLA Zhang, Ziwen,et al."Caspase-3-mediated GSDME induced Pyroptosis in breast cancer cells through the ROS/JNK signalling pathway".JOURNAL OF CELLULAR AND MOLECULAR MEDICINE (2021).

入库方式: OAI收割

来源:合肥物质科学研究院

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