Green Tea and Cancer Prevention

被引:122
作者
Yang, Chung S. [1 ]
Wang, Xin [1 ]
机构
[1] Rutgers State Univ, Ernest Mario Sch Pharm, Dept Biol Chem, Piscataway, NJ 08854 USA
来源
NUTRITION AND CANCER-AN INTERNATIONAL JOURNAL | 2010年 / 62卷 / 07期
关键词
GROWTH-FACTOR RECEPTOR; INDUCED LUNG TUMORIGENESIS; PROSTATE CARCINOMA-CELLS; (-)-EPIGALLOCATECHIN GALLATE; A/J MICE; BLACK TEA; POLYPHENOL (-)-EPIGALLOCATECHIN-3-GALLATE; BREAST-CANCER; SIGNALING PATHWAYS; COLORECTAL-CANCER;
D O I
10.1080/01635581.2010.509536
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Extracts of green tea and green tea polyphenols have exhibited inhibitory effects against the formation and development of tumors at different organ sites in animals. These include animal models for skin, lung, oral cavity, esophagus, stomach, intestine, colon, liver, pancreas, bladder, mammary gland, and prostate cancers. In addition to suppressing cell proliferation, promoting apoptosis, and modulating signaling transduction, green tea polyphenols, especially (-)-epigallocatechin-3-gallate, also inhibit cell invasion, angiogenesis, and metastasis. This article reviews data on the cancer preventive activities of green tea polyphenols, possible mechanisms involved, and the relationship between green tea consumption and human cancer risk.
引用
收藏
页码:931 / 937
页数:7
相关论文
共 81 条
[1]   (-)-epigallocatechin gallate causes internalization of the epidermal growth factor receptor in human colon cancer cells [J].
Adachi, Seiji ;
Nagao, Tomokazu ;
To, Satoshi ;
Joe, Andrew K. ;
Shimizu, Masahito ;
Matsushima-Nishiwaki, Rie ;
Kozawa, Osamu ;
Moriwaki, Hisataka ;
Maxfield, Frederick R. ;
Weinstein, I. Bernard .
CARCINOGENESIS, 2008, 29 (10) :1986-1993
[2]   The inhibitory effect of (-)-epigallocatechin gallate on activation of the epidermal growth factor receptor is associated with altered lipid order in HT29 colon cancer cells [J].
Adachi, Seiji ;
Nagao, Tomokazu ;
Ingolfsson, Helgi I. ;
Maxfield, Frederick R. ;
Andersen, Olaf S. ;
Kopelovich, Levy ;
Weinstein, I. Bernard .
CANCER RESEARCH, 2007, 67 (13) :6493-6501
[3]   Oral consumption of green tea polyphenols inhibits insulin-like growth factor-i-induced signaling in an autochthonous mouse model of prostate cancer [J].
Adhami, VM ;
Siddiqui, IA ;
Ahmad, N ;
Gupta, S ;
Mukhtar, H .
CANCER RESEARCH, 2004, 64 (23) :8715-8722
[4]   Protective effects of green tea extracts (polyphenon E and EGCG) on human cervical lesions [J].
Ahn, WS ;
Yoo, J ;
Huh, SW ;
Kim, CK ;
Lee, JM ;
Namkoong, SE ;
Bae, SM ;
Lee, IP .
EUROPEAN JOURNAL OF CANCER PREVENTION, 2003, 12 (05) :383-390
[5]   Green tea polyphenol (-)-epigallocatechin 3-gallate inhibits MMP-2 secretion and MT1-MMP-driven migration in glioblastoma cells [J].
Annabi, B ;
Lachambre, MP ;
Bousquet-Gagnon, N ;
Pagé, M ;
Gingras, D ;
Béliveau, R .
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH, 2002, 1542 (1-3) :209-220
[6]   The chemistry of tea flavonoids [J].
Balentine, DA ;
Wiseman, SA ;
Bouwens, LCM .
CRITICAL REVIEWS IN FOOD SCIENCE AND NUTRITION, 1997, 37 (08) :693-704
[7]   Chemoprevention of human prostate cancer by oral administration of green tea catechins in volunteers with high-grade prostate intraepithelial neoplasia: A preliminary report from a one-year proof-of-principle study [J].
Bettuzzi, S ;
Brausi, M ;
Rizzi, F ;
Castagnetti, G ;
Peracchia, G ;
Corti, A .
CANCER RESEARCH, 2006, 66 (02) :1234-1240
[8]   The green tea catechins, (-)-epigallocatechin-3-gallate (EGCG) and (-)-epicatechin-3-gallate (ECG), inhibit HGF/Met signaling in immortalized and tumorigenic breast epithelial cells [J].
Bigelow, RLH ;
Cardelli, JA .
ONCOGENE, 2006, 25 (13) :1922-1930
[9]   Met, metastasis, motility and more [J].
Birchmeier, C ;
Birchmeier, W ;
Gherardi, E ;
Vande Woude, GF .
NATURE REVIEWS MOLECULAR CELL BIOLOGY, 2003, 4 (12) :915-925
[10]   Green tea consumption, genetic susceptibility, PAH-rich smoky coal, and the risk of lung cancer [J].
Bonner, MR ;
Rothman, N ;
Mumford, JL ;
He, XZ ;
Shen, M ;
Welch, R ;
Yeager, M ;
Chanock, S ;
Caporaso, N ;
Lan, Q .
MUTATION RESEARCH-GENETIC TOXICOLOGY AND ENVIRONMENTAL MUTAGENESIS, 2005, 582 (1-2) :53-60