Indole-3-Carbinol Inhibits Nasopharyngeal Carcinoma

被引:5
作者
Zhu, Wei [1 ,2 ]
Li, Wenxue [2 ]
Yang, Guangyu [2 ]
Zhang, Quanxin [2 ]
Li, Ming [1 ]
Yang, Xingfen [3 ]
机构
[1] Nanfang Med Univ, Dept Biotechnol, Guangzhou 510515, Guangdong, Peoples R China
[2] Guangzhou Ctr Dis Control & Prevent, Dept Toxicol, Guangzhou, Guangdong, Peoples R China
[3] Guangdong Ctr Dis Control & Prevent, Guangzhou, Guangdong, Peoples R China
基金
中国国家自然科学基金; 国家高技术研究发展计划(863计划);
关键词
caspase-3; caspase-9; human nasopharyngeal carcinoma cell; indole-3-carbinol; DNA-ADDUCTS; CANCER-RISK; CELL-LINE; APOPTOSIS; CHEMOTHERAPY; MICE; TUMORIGENESIS; ACTIVATION; CASPASES; STRESS;
D O I
10.1177/1091581809356481
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
This study explored the effects of indole-3-carbinol on the proliferation of human nasopharyngeal carcinoma, both in vitro and in vivo, and the underlying mechanisms in inducing apoptosis of CNE1 cells. Proliferation, apoptosis, malondialdehyde, superoxide dismutase, glutathione peroxidase, expressions of caspase-9, and caspase-3 in human nasopharyngeal carcinoma cells CNE1 were examined. Indole-3-carbinol suppressed proliferation, induced apoptosis, decreased malondialdehyde level, increased the activity of superoxide dismutase and glutathione peroxidase, and up-regulated the expression of active fragments of caspase-9 and caspase-3 both in vitro and in vivo. It was concluded that indole-3-carbinol could inhibit proliferation and induce apoptosis of CNE1 cells and inhibit tumor growth in mice. Increased activity of superoxide dismutase and glutathione peroxidase and activated expression of caspase-9 and caspase-3 were also observed in indole-3-carbinol-treated tumors or tumor cells, suggesting that stress-and apoptosis-related molecules are involved in the indole-3-carbinol-induced apoptosis and inhibition of tumor growth.
引用
收藏
页码:185 / 192
页数:8
相关论文
共 33 条
[1]   Molecular targets and anticancer potential of indole-3-carbinol and its derivatives [J].
Aggarwal, BB ;
Ichikawa, H .
CELL CYCLE, 2005, 4 (09) :1201-1215
[2]  
Ali H, 2000, ONCOLOGY-NY, V14, P1223
[3]   UNDIFFERENTIATED NASOPHARYNGEAL CANCER (UCNT) - CURRENT DIAGNOSTIC AND THERAPEUTIC ASPECTS [J].
ALTUN, M ;
FANDI, A ;
DUPUIS, O ;
CVITKOVIC, E ;
KRAJINA, Z ;
ESCHWEGE, F .
INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS, 1995, 32 (03) :859-877
[4]   Inhibition of cigarette smoke-related DNA adducts in rat tissues by indole-3-carbinol [J].
Arif, JM ;
Gairola, CG ;
Kelloff, GJ ;
Lubet, RA ;
Gupta, RC .
MUTATION RESEARCH-FUNDAMENTAL AND MOLECULAR MECHANISMS OF MUTAGENESIS, 2000, 452 (01) :11-18
[5]  
Chan ATC, 1998, CANCER-AM CANCER SOC, V82, P1003, DOI 10.1002/(SICI)1097-0142(19980315)82:6<1003::AID-CNCR1>3.0.CO
[6]  
2-F
[7]  
CHOO R, 1991, CANCER, V68, P2120, DOI 10.1002/1097-0142(19911115)68:10<2120::AID-CNCR2820681005>3.0.CO
[8]  
2-7
[9]   Comprehensive Profiling of Epstein-Barr Virus MicroRNAs in Nasopharyngeal Carcinoma [J].
Cosmopoulos, Katherine ;
Pegtel, Michiel ;
Hawkins, Jared ;
Moffett, Howell ;
Novina, Carl ;
Middeldorp, Jaap ;
Thorley-Lawson, David A. .
JOURNAL OF VIROLOGY, 2009, 83 (05) :2357-2367
[10]   Low Concentrations of Diindolyl methane, a Metabolite of Indole-3-Carbinol, Protect against Oxidative Stress in a BRCA1-Dependent Manner [J].
Fan, Saijun ;
Meng, Qinghui ;
Saha, Tapas ;
Sarkar, Fazlul H. ;
Rosen, Eliot M. .
CANCER RESEARCH, 2009, 69 (15) :6083-6091