中国科学院机构知识库网格
Chinese Academy of Sciences Institutional Repositories Grid
Trichosanthin induced apoptosis in HL-60 cells via mitochondrial and endoplasmic reticulumstress signaling pathways

文献类型:期刊论文

作者Li, J; Xia, XC; Ke, YB; Nie, HL; Smith, MA; Zhu, XW
刊名BIOCHIMICA ET BIOPHYSICA ACTA-GENERAL SUBJECTS
出版日期2007
卷号1770期号:8页码:1169-1180
关键词trichosanthin apoptosis caspase mitochondria endoplasmic reticulum stress
通讯作者Nie, HL (reprint author), Chinese Acad Sci, Grad Sch, Shanghai Inst Biol Sci, Inst Biochem & Cell Biol, 320 Yue Yang Rd, Shanghai 200031, Peoples R China.,hlnie@sibs.ac.cn ; Xiongwei.zhu@case.edu
英文摘要Trichosanthin (TCS), a traditional Chinese medicine, exerts antitumor activities by inducing apoptosis in many different tumor cell lines. However, the mechanisms remain obscure. The present study focused on various caspase pathways that may be involved in TCS-induced apoptosis in leukemia HL-60 cells. Key caspases in both intrinsic and extrinsic pathways including caspase-8, -9 and -3 were activated upon TCS treatment. Additionally, TCS treatment induced upregulation of BiP and CHOP and also activated caspase-4, which for the first time strongly supported the involvement of endoplasmic reticulum stress pathway in TCS-induced apoptosis. Interestingly, although caspase-8 was activated, Fas/Fas ligand pathway vas not involved as evidenced by a lack of induction of Fas or Fas ligand and a lack of inhibitory effect of anti-Fas blocking antibody on TCS-induced apoptosis. Instead, caspase-8 was activated in a caspase-9 and -4 dependent manner. The involvement of mitochondria was demonstrated by the reduction of mitochondrial membrane potential and release of cytochrome c and Smac besides the activation of caspase-9. Further investigation confirmed that caspase-3 was the major executioner caspase downstream to caspase-9, -4 and -8. Taken together, our results suggested that TCS-induced apoptosis in HL-60 cells was mainly mediated by mitochondrial and ER stress signaling pathways via caspase-3. (C) 2007 Elsevier B.V. All rights reserved.
学科主题Biochemistry & Molecular Biology; Biophysics
类目[WOS]Biochemistry & Molecular Biology ; Biophysics
关键词[WOS]RIBOSOME-INACTIVATING PROTEIN ; CYTOCHROME-C RELEASE ; CHORIOCARCINOMA CELLS ; DEATH RECEPTORS ; LEUKEMIA-CELLS ; JURKAT CELLS ; STRESS ; ACTIVATION ; CASPASE ; INDUCTION
收录类别SCI
语种英语
WOS记录号WOS:000248501000011
版本出版稿
源URL[http://202.127.25.143/handle/331003/1587]  
专题上海生化细胞研究所_上海生科院生化细胞研究所
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GB/T 7714
Li, J,Xia, XC,Ke, YB,et al. Trichosanthin induced apoptosis in HL-60 cells via mitochondrial and endoplasmic reticulumstress signaling pathways[J]. BIOCHIMICA ET BIOPHYSICA ACTA-GENERAL SUBJECTS,2007,1770(8):1169-1180.
APA Li, J,Xia, XC,Ke, YB,Nie, HL,Smith, MA,&Zhu, XW.(2007).Trichosanthin induced apoptosis in HL-60 cells via mitochondrial and endoplasmic reticulumstress signaling pathways.BIOCHIMICA ET BIOPHYSICA ACTA-GENERAL SUBJECTS,1770(8),1169-1180.
MLA Li, J,et al."Trichosanthin induced apoptosis in HL-60 cells via mitochondrial and endoplasmic reticulumstress signaling pathways".BIOCHIMICA ET BIOPHYSICA ACTA-GENERAL SUBJECTS 1770.8(2007):1169-1180.

入库方式: OAI收割

来源:上海生物化学与细胞生物学研究所

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