Trichosanthin induced apoptosis in HL-60 cells via mitochondrial and endoplasmic reticulumstress signaling pathways

	Trichosanthin induced apoptosis in HL-60 cells via mitochondrial and endoplasmic reticulumstress signaling pathways
	Li, J; Xia, XC; Ke, YB; Nie, HL; Smith, MA; Zhu, XW
刊名	BIOCHIMICA ET BIOPHYSICA ACTA-GENERAL SUBJECTS
	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
内容类型	期刊论文
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.