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
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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 |
推荐引用方式 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. |
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