N-Acetyl cysteine and caffeic acid phenethyl ester sensitize astrocytoma cells to Fas-mediated cell death in a redox-dependent manner

被引：18
作者：
Choi, Kyungsun
Han, Young-Hee
Choi, Chulhee
机构：
[1] Korea Adv Inst Sci & Technol, Dept Brain & Bioengn, Lab Computat Cell Biol, Taejon 305701, South Korea
[2] Korea Adv Inst Sci & Technol, Grad Sch Med Sci & Engn, Taejon 305701, South Korea
[3] Korea Adv Inst Sci & Technol, Inst BioCentury, Taejon 305701, South Korea
来源：
CANCER LETTERS | 2007年 / 257卷 / 01期
关键词：
apoptosis; caffeic acid phenethyl ester; fas; reactive oxygen species; n-acetyl cysteine;
D O I：
10.1016/j.canlet.2007.07.006
中图分类号：
R73 [肿瘤学];
学科分类号：
100214 ;
摘要：
In this study, we investigated the role of reactive oxygen species (ROS) in Fas-induced cell death in human astrocytoma cells. Fas activation increased intracellular ROS levels in a NADPH oxidase- and caspase-dependent manner. ROS inhibitors such as N-acetyl cysteine (NAC) and caffeic acid phenethyl ester (CAPE) dramatically sensitized astocytoma cells to Fas-induced loss of mitochondrial transmembrane potential and subsequent cell death, which were abrogated by pretreatment with z-VAD-fmk, a broad-spectrum caspase inhibitor. These results collectively indicate that NAC and CAPE sensitize astrocytoma cells to Fas-induced apoptosis in a redox-dependent manner, suggesting a potential use in the treatment of malignant brain tumors. (C) 2007 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码：79 / 86
页数：8
相关论文
共 47 条
[1]   Caffeic acid phenethyl ester blocks apoptosis induced by low potassium in cerebellar granule cells [J].
Amodio, R ;
De Ruvo, C ;
Di Matteo, V ;
Poggi, A ;
Di Santo, A ;
Martelli, N ;
Lorenzet, R ;
Rotilio, D ;
Cacchio, M ;
Esposito, E .
INTERNATIONAL JOURNAL OF DEVELOPMENTAL NEUROSCIENCE, 2003, 21 (07) :379-389
[2]   Potentiation of Fas-mediated apoptosis by attenuated production of mitochondria-derived reactive oxygen species [J].
Aronis, A ;
Melendez, JA ;
Golan, O ;
Shilo, S ;
Dicter, N ;
Tirosh, O .
CELL DEATH AND DIFFERENTIATION, 2003, 10 (03) :335-344
[3]   Glutathione levels determine apoptosis in macrophages [J].
Boggs, SE ;
McCormick, TS ;
Lapetina, EG .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1998, 247 (02) :229-233
[4]   Signalling apoptosis: a radical approach [J].
Carmody, RJ ;
Cotter, TG .
REDOX REPORT, 2001, 6 (02) :77-90
[5]   The antioxidant caffeic acid phenethyl ester induces apoptosis associated with selective scavenging of hydrogen peroxide in human leukemic HL-60 cells [J].
Chen, YJ ;
Shiao, MS ;
Wang, SY .
ANTI-CANCER DRUGS, 2001, 12 (02) :143-149
[6]  
CHIAO C, 1995, CANCER RES, V55, P3576
[7]   Fas ligand/Fas system in the brain: regulator of immune and apoptotic responses [J].
Choi, C ;
Benveniste, EN .
BRAIN RESEARCH REVIEWS, 2004, 44 (01) :65-81
[8]   Caspase-1 mediates Fas-induced apoptosis and is up-regulated by interferon-γ in human astrocytoma cells [J].
Choi, C ;
Jeong, E ;
Benveniste, EN .
JOURNAL OF NEURO-ONCOLOGY, 2004, 67 (1-2) :167-176
[9]   Tumor necrosis factor-related apoptosis-inducing ligand induces caspase-dependent interleukin-8 expression and apoptosis in human astroglioma cells [J].
Choi, C ;
Kutsch, O ;
Park, J ;
Zhou, T ;
Seol, DW ;
Benveniste, EN .
MOLECULAR AND CELLULAR BIOLOGY, 2002, 22 (03) :724-736
[10]   Ginsenosides compound K and Rh2 inhibit tumor necrosis factor-α-induced activation of the NF-κB and JNK pathways in human astroglial cells [J].
Choi, Kyungsun ;
Kim, Myungsun ;
Ryu, Jeonghee ;
Choi, Chulhee .
NEUROSCIENCE LETTERS, 2007, 421 (01) :37-41
12345