Modulation of cell signal transduction by tea and ginger

Dietary Modulation of Cell Signaling Pathways

Volumn , Issue , 2008, Pages 45-74

  Bode, Ann M ^a   Dong, Zigang ^a  

^a UNIVERSITY OF MINNESOTA   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

EID: 85055474192     PISSN: None     EISSN: None     Source Type: Book    
DOI: None     Document Type: Chapter

References (245)

1. Hong, W.K., General keynote: the impact of cancer chemoprevention, Gynecol Oncol, 88, S56, 2003.
2. Bode, A.M. and Dong, Z., Apoptosis induction by arsenic: mechanisms of actions and possible clinical applications for treating therapy-resistant cancers, Drug Resistance Updates, 3, 21, 2000.
3. Bode, A.M. and Dong, Z., The paradox of arsenic: molecular mechanisms of cell transformation and chemotherapeutic effects, Crit Rev Oncol Hematol, 42, 5, 2002.
4. Bode, A.M. and Dong, Z., Signal transduction pathways: targets for green and black tea polyphenols, J Biochem Mol Biol, 36, 66, 2003.
5. Bode, A.M. and Dong, Z., Beneficial effects of resveratrol, in Phytochemicals in Health and Disease, Y. Bao and R. Fenwick, Eds., Marcel Dekker, New York, 257, 2004.
6. Bode, A.M. and Dong, Z., Signal transduction pathways in cancer development and as targets for cancer prevention, Prog Nucleic Acid Res Mol Biol, 79, 237, 2005.
7. Angel, P., et al., The jun proto-oncogene is positively autoregulated by its product, Jun/AP-1, Cell, 55, 875, 1988.
8. Davis, R.J., MAPKs: new JNK expands the group, Trends Biochem Sci, 19, 470, 1994.
9. Kallunki, T., et al., JNK2 contains a specificity-determining region responsible for efficient c-Jun binding and phosphorylation, Genes Dev, 8, 2996, 1994.
10. Sanchez, I., et al., Role of SAPK/ERK kinase-1 in the stress-activated pathway regulating transcription factor c-Jun, Nature, 372, 794, 1994.
11. Eferl, R. and Wagner, E.F., AP-1: a double-edged sword in tumorigenesis, Nat Rev Cancer, 3, 859, 2003.
12. Angel, P. and Karin, M., The role of Jun, Fos and the AP-1 complex in cell-proliferation and transformation, Biochim Biophys Acta, 1072, 129, 1991.
13. Dong, Z., et al., Progressive elevation of AP-1 activity during preneoplastic to neoplastic progression as modeled in mouse JB6 cell variants, Int J Oncol, 7, 359, 1995.
14. Dong, Z., et al., Blocking of tumor promoter-induced AP-1 activity inhibits induced transformation in JB6 mouse epidermal cells, Proc Natl Acad Sci USA, 91, 609, 1994.
15. Barthelman, M., et al., Inhibitory effects of perillyl alcohol on UVB-induced murine skin cancer and AP-1 transactivation, Cancer Res, 58, 711, 1998.
16. Huang, C., et al., Blocking activator protein-1 activity, but not activating retinoic acid response element, is required for the antitumor promotion effect of retinoic acid, Proc Natl Acad Sci USA, 94, 5826, 1997.
17. Li, J.J., et al., Inhibition of tumor promoter-induced transformation by retinoids that transrepress AP-1 without transactivating retinoic acid response element, Cancer Res, 56, 483, 1996.
18. Huang, C., et al., Inhibitory effects of ascorbic acid on AP-1 activity and transformation of JB6 cells, Int J Oncol, 8, 389, 1996.
19. Dong, Z., et al., A dominant negative mutant of jun blocking 12-O-tetradecanoylphorbol-13-acetate-induced invasion in mouse keratinocytes, Mol Carcinog, 19, 204, 1997.
20. Baldwin, A.S., Jr., The NF-kappa B and I kappa B proteins: new discoveries and insights, Annu Rev Immunol, 14, 649, 1996.
21. Schulze-Osthoff, K., et al., Regulation of NF-kappa B activation by MAP kinase cascades, Immunobiology, 198, 35, 1997.
22. Gilmore, T.D., Clinically relevant findings [editorial], J Clin Invest, 100, 2935, 1997.
23. Li, J.J., et al., Inhibitors of both nuclear factor-kappa B and activator protein-1 activation block the neoplastic transformation response, Cancer Res, 57, 3569, 1997.
24. Cowley, S., et al., Activation of MAP kinase kinase is necessary and sufficient for PC12 differentiation and for transformation of NIH 3T3 cells, Cell, 77, 841, 1994.
25. Huang, C., et al., Arsenic induces apoptosis through a c-Jun NH2-terminal kinasedependent, p53-independent pathway, Cancer Res, 59, 3053, 1999.
26. Yang, C.S., et al., Possible mechanisms of the cancer-preventive activities of green tea, Mol Nutr Food Res, 50, 170, 2006.
27. Yang, C.S., et al., Molecular targets for the cancer preventive activity of tea polyphenols, Mol Carcinog, 45, 431, 2006.
28. Mizuno, H., et al., Theaflavin-3,3′-digallate induces epidermal growth factor receptor downregulation, Mol Carcinog, 45, 204, 2006.
29. Na, H.K. and Surh, Y.J., Intracellular signaling network as a prime chemopreventive target of (-)-epigallocatechin gallate, Mol Nutr Food Res, 50, 152, 2006.
30. Khan, N., et al., Targeting multiple signaling pathways by green tea polyphenol (-)-epigallocatechin-3-gallate, Cancer Res, 66, 2500, 2006.
31. Bode, A.M. and Dong, Z., Molecular and cellular targets, Mol Carcinog, 45, 422, 2006.
32. Trevisanato, S.I. and Kim, Y.I., Tea and health, Nutr Rev, 58, 1, 2000.
33. Huang, M.T., et al., Inhibitory effect of topical application of a green tea polyphenol fraction on tumor initiation and promotion in mouse skin, Carcinogenesis, 13, 947, 1992.
34. Yang, C.S. and Wang, Z.Y., Tea and cancer, J Natl Cancer Inst, 85, 1038, 1993.
35. Yang, C.S., Inhibition of carcinogenesis by tea, Nature, 389, 134, 1997.
36. Katiyar, S.K. and Mukhtar, H., Tea in chemoprevention of cancer: epidemiologic and experimental studies, Int J Oncol, 8, 221, 1996.
37. Dreosti, I.E., et al., Inhibition of carcinogenesis by tea: the evidence from experimental studies, Crit Rev Food Sci Nutr, 37, 761, 1997.
38. Ju, J., et al., Inhibition of intestinal tumorigenesis in Apcmin/+ mice by (-)-epigallocatechin-3-gallate, the major catechin in green tea, Cancer Res, 65, 10623, 2005.
39. Nakachi, K., et al., Influence of drinking green tea on breast cancer malignancy among Japanese patients, Jpn J Cancer Res, 89, 254, 1998.
40. Ji, B.T., et al., Green tea consumption and the risk of pancreatic and colorectal cancers, Int J Cancer, 70, 255, 1997.
41. Inoue, M., et al., Tea and coffee consumption and the risk of digestive tract cancers: data from a comparative case-referent study in Japan, Cancer Causes Control, 9, 209, 1998.
42. Tan, M., et al., Effects of (-)epigallocatechin gallate and thymoquinone on proliferation of a PANC-1 cell line in culture, Biomed Sci Instrum, 42, 363, 2006.
43. Kim, J., et al., Suppression of Wnt signaling by the green tea compound (-)-epigallocatechin 3-gallate (EGCG) in invasive breast cancer cells. Requirement of the transcriptional repressor HBP1, J Biol Chem, 281, 10865, 2006.
44. Richards, L.R., et al., The physiological effect of conventional treatment with epigallocatechin-3-gallate, thymoquinone, and tannic acid on the LNCaP cell line, Biomed Sci Instrum, 42, 357, 2006.
45. Siddiqui, I.A., et al., Inhibition of CWR22Rnu1 tumor growth and PSA secretion in athymic nude mice by green and black teas, Carcinogenesis, 27, 833, 2006.
46. Jatoi, A., et al., A phase II trial of green tea in the treatment of patients with androgen independent metastatic prostate carcinoma, Cancer, 97, 1442, 2003.
47. Pisters, K.M., et al., Phase I trial of oral green tea extract in adult patients with solid tumors, J Clin Oncol, 19, 1830, 2001.
48. Jankun, J., et al., Why drinking green tea could prevent cancer, Nature, 387, 561, 1997.
49. Graham, H.N., Green tea composition, consumption, and polyphenol chemistry, Prev Med, 21, 334, 1992.
50. Bode, A.M. and Dong, Z., Signal transduction pathways: targets for chemoprevention of skin cancer, Lancet Oncol., 1, 181, 2000.
51. Chen, N.Y., et al., Inhibition of arsenite-induced apoptosis and AP-1 activity by epigallocatechin-3-gallate and theaflavins, J Environ Pathol Toxicol Oncol, 19, 287, 2000.
52. Dong, Z., et al., Inhibition of tumor promoter-induced activator protein 1 activation and cell transformation by tea polyphenols, (-)-epigallocatechin gallate, and theaflavins, Cancer Res, 57, 4414, 1997.
53. Ahn, H.Y., et al., Epigallocathechin-3 gallate selectively inhibits the PDGF-BBinduced intracellular signaling transduction pathway in vascular smooth muscle cells and inhibits transformation of sis-transfected NIH 3T3 fibroblasts and human glioblastoma cells (A172), Mol Biol Cell, 10, 1093, 1999.
54. Barthelman, M., et al., (-)-Epigallocatechin-3-gallate inhibition of ultraviolet B-induced AP-1 activity, Carcinogenesis, 19, 2201, 1998.
55. Nomura, M., et al., Inhibition of ultraviolet B-induced AP-1 activation by theaflavins from black tea, Mol Carcinog, 28, 148, 2000.
56. Chen, W., et al., Inhibition of ultraviolet B-induced c-fos gene expression and p38 mitogen-activated protein kinase activation by (-)-epigallocatechin gallate in a human keratinocyte cell line, Mol Carcinog, 24, 79, 1999.
57. Chung, J.Y., et al., Inhibition of activator protein 1 activity and cell growth by purified green tea and black tea polyphenols in H-ras-transformed cells: structure-activity relationship and mechanisms involved, Cancer Res, 59, 4610, 1999.
58. Peng, G., et al., Anti-proliferative effects of green tea polyphenol EGCG on Ha-Ras-induced transformation of intestinal epithelial cells, Cancer Lett, 238, 260, 2006.
59. Shimizu, M., et al., (-)-Epigallocatechin gallate and polyphenon E inhibit growth and activation of the epidermal growth factor receptor and human epidermal growth factor receptor-2 signaling pathways in human colon cancer cells, Clin Cancer Res, 11, 2735, 2005.
60. Kim, H.S., et al., EGCG blocks tumor promoter-induced MMP-9 expression via suppression of MAPK and AP-1 activation in human gastric AGS cells, Anticancer Res, 24, 747, 2004.
61. Syed, D.N., et al., Green tea polyphenol EGCG suppresses cigarette smoke condensate- induced NF-kappaB activation in normal human bronchial epithelial cells, Oncogene, 26, 673, 2007.
62. Kim, M., et al., (-)-Epigallocatechin-3-gallate promotes pro-matrix metalloproteinase-7 production via activation of the JNK1/2 pathway in HT-29 human colorectal cancer cells, Carcinogenesis, 26, 1553, 2005.
63. Afaq, F., et al., Inhibition of ultraviolet B-mediated activation of nuclear factor kappaB in normal human epidermal keratinocytes by green tea constituent (-)-epigallocatechin-3-gallate, Oncogene, 22, 1035, 2003.
64. Nomura, M., et al., Inhibition of 12-O-tetradecanoylphorbol-13-acetate-induced NF-kappaB activation by tea polyphenols, (-)-epigallocatechin gallate and theaflavins, Carcinogenesis, 21, 1885, 2000.
65. Nam, S., et al., Ester bond-containing tea polyphenols potently inhibit proteasome activity in vitro and in vivo, J Biol Chem, 276, 13322, 2001.
66. Ahmad, N., et al., Green tea polyphenol epigallocatechin-3-gallate differentially modulates nuclear factor kappaB in cancer cells versus normal cells, Arch Biochem Biophys, 376, 338, 2000.
67. Xia, J., et al., UV-induced NF-kappaB activation and expression of IL-6 is attenuated by (-)-epigallocatechin-3-gallate in cultured human keratinocytes in vitro, Int J Mol Med, 16, 943, 2005.
68. Meeran, S.M., et al., (-)-Epigallocatechin-3-gallate prevents photocarcinogenesis in mice through interleukin-12-dependent DNA repair, Cancer Res, 66, 5512, 2006.
69. Glei, M. and Pool-Zobel, B.L., The main catechin of green tea, (-)-epigallocatechin-3-gallate (EGCG), reduces bleomycin-induced DNA damage in human leucocytes, Toxicol In Vitro, 20, 295, 2006.
70. Vivanco, I. and Sawyers, C.L., The phosphatidylinositol 3-kinase AKT pathway in human cancer, Nat Rev Cancer, 2, 489, 2002.
71. Sen, P., et al., Tea polyphenol epigallocatechin 3-gallate impedes the anti-apoptotic effects of low-grade repetitive stress through inhibition of Akt and NFkappaB survival pathways, FEBS Lett, 580, 278, 2006.
72. Nomura, M., et al., Inhibitory mechanisms of tea polyphenols on the ultraviolet B-activated phosphatidylinositol 3-kinase-dependent pathway, J Biol Chem, 276, 46624, 2001.
73. Pianetti, S., et al., Green tea polyphenol epigallocatechin-3 gallate inhibits Her-2/neu signaling, proliferation, and transformed phenotype of breast cancer cells, Cancer Res, 62, 652, 2002.
74. Bigelow, R.L. and Cardelli, J.A., The green tea catechins, (-)-epigallocatechin-3-gallate (EGCG) and (-)-epicatechin-3-gallate (ECG), inhibit HGF/Met signaling in immortalized and tumorigenic breast epithelial cells, Oncogene, 25, 1922, 2006.
75. Rodriguez, S.K., et al., Green tea catechin, epigallocatechin-3-gallate, inhibits vascular endothelial growth factor angiogenic signaling by disrupting the formation of a receptor complex, Int J Cancer, 118, 1635, 2006.
76. Zhang, Q., et al., Green tea extract and (-)-epigallocatechin-3-gallate inhibit hypoxia- and serum-induced HIF-1alpha protein accumulation and VEGF expression in human cervical carcinoma and hepatoma cells, Mol Cancer Ther, 5, 1227, 2006.
77. Sah, J.F., et al., Epigallocatechin-3-gallate inhibits epidermal growth factor receptor signaling pathway: evidence for direct inhibition of ERK1/2 and AKT kinases, J Biol Chem, 279, 12755, 2004.
78. Siddiqui, I.A., et al., Modulation of phosphatidylinositol-3-kinase/protein kinase B- and mitogen-activated protein kinase-pathways by tea polyphenols in human prostate cancer cells, J Cell Biochem, 91, 232, 2004.
79. Wu, C.C., et al., Upregulation of heme oxygenase-1 by epigallocatechin-3-gallate via the phosphatidylinositol 3-kinase/Akt and ERK pathways, Life Sci, 78, 2889, 2006.
80. Guo, S., et al., Microarray-assisted pathway analysis identifies mitogen-activated protein kinase signaling as a mediator of resistance to the green tea polyphenol epigallocatechin 3-gallate in her-2/neu-overexpressing breast cancer cells, Cancer Res, 66, 5322, 2006.
81. Turini, M.E. and DuBois, R.N., Cyclooxygenase-2: a therapeutic target, Annu Rev Med, 53, 35, 2002.
82. Subbaramaiah, K. and Dannenberg, A.J., Cyclooxygenase 2: a molecular target for cancer prevention and treatment, Trends Pharmacol Sci, 24, 96, 2003.
83. Prescott, S.M. and Fitzpatrick, F.A., Cyclooxygenase-2 and carcinogenesis, Biochim Biophys Acta, 1470, M69, 2000.
84. Sano, H., et al., Expression of cyclooxygenase-1 and -2 in human colorectal cancer, Cancer Res, 55, 3785, 1995.
85. Eberhart, C.E., et al., Up-regulation of cyclooxygenase 2 gene expression in human colorectal adenomas and adenocarcinomas, Gastroenterology, 107, 1183, 1994.
86. Kutchera, W., et al., Prostaglandin H synthase 2 is expressed abnormally in human colon cancer: evidence for a transcriptional effect, Proc Natl Acad Sci USA, 93, 4816, 1996.
87. Hwang, D., et al., Expression of cyclooxygenase-1 and cyclooxygenase-2 in human breast cancer, J Natl Cancer Inst, 90, 455, 1998.
88. Subbaramaiah, K., et al., Transcription of cyclooxygenase-2 is enhanced in transformed mammary epithelial cells, Cancer Res, 56, 4424, 1996.
89. Wolff, H., et al., Expression of cyclooxygenase-2 in human lung carcinoma, Cancer Res, 58, 4997, 1998.
90. Hida, T., et al., Increased expression of cyclooxygenase 2 occurs frequently in human lung cancers, specifically in adenocarcinomas, Cancer Res, 58, 3761, 1998.
91. van Rees, B.P., et al., Cyclooxygenase-2 expression during carcinogenesis in the human stomach, J Pathol, 196, 171, 2002.
92. Ristimaki, A., et al., Expression of cyclooxygenase-2 in human gastric carcinoma, Cancer Res, 57, 1276, 1997.
93. Chan, G., et al., Cyclooxygenase-2 expression is up-regulated in squamous cell carcinoma of the head and neck, Cancer Res, 59, 991, 1999.
94. Gallo, O., et al., Cyclooxygenase-2 pathway correlates with VEGF expression in head and neck cancer: implications for tumor angiogenesis and metastasis, Neoplasia, 3, 53, 2001.
95. Mestre, J.R., et al., Inhibition of cyclooxygenase-2 expression: an approach to preventing head and neck cancer, Ann NY Acad Sci, 889, 62, 1999.
96. Tucker, O.N., et al., Cyclooxygenase-2 expression is up-regulated in human pancreatic cancer, Cancer Res, 59, 987, 1999.
97. Tong, B.J., et al., Heightened expression of cyclooxygenase-2 and peroxisome proliferator- activated receptor-delta in human endometrial adenocarcinoma, Neoplasia, 2, 483, 2000.
98. Gaffney, D.K., et al., Elevated cyclooxygenase-2 expression correlates with diminished survival in carcinoma of the cervix treated with radiotherapy, Int J Radiat Oncol Biol Phys, 49, 1213, 2001.
99. Grubbs, C.J., et al., Celecoxib inhibits N-butyl-N-(4-hydroxybutyl)-nitrosamineinduced urinary bladder cancers in male B6D2F1 mice and female Fischer-344 rats, Cancer Res, 60, 5599, 2000.
100. Grossman, E.M., et al., The role of cyclooxygenase enzymes in the growth of human gall bladder cancer cells, Carcinogenesis, 21, 1403, 2000.
101. Denkert, C., et al., Expression of cyclooxygenase 2 in human malignant melanoma, Cancer Res, 61, 303, 2001.
102. Buckman, S.Y., et al., COX-2 expression is induced by UVB exposure in human skin: implications for the development of skin cancer, Carcinogenesis, 19, 723, 1998.
103. An, K.P., et al., Cyclooxygenase-2 expression in murine and human nonmelanoma skin cancers: implications for therapeutic approaches, Photochem Photobiol, 76, 73, 2002.
104. Athar, M., et al., Ultraviolet B(UVB)-induced cox-2 expression in murine skin: an immunohistochemical study, Biochem Biophys Res Commun, 280, 1042, 2001.
105. Lee, J.L., et al., Cyclooxygenases in the skin: pharmacological and toxicological implications, Toxicol Appl Pharmacol, 192, 294, 2003.
106. Tiano, H.F., et al., Deficiency of either cyclooxygenase (COX)-1 or COX-2 alters epidermal differentiation and reduces mouse skin tumorigenesis, Cancer Res, 62, 3395, 2002.
107. Bol, D.K., et al., Cyclooxygenase-2 overexpression in the skin of transgenic mice results in suppression of tumor development, Cancer Res, 62, 2516, 2002.
108. Hussain, T., et al., Green tea constituent epigallocatechin-3-gallate selectively inhibits COX-2 without affecting COX-1 expression in human prostate carcinoma cells, Int J Cancer, 113, 660, 2005.
109. Lee, S.J., et al., Inhibition of inducible nitric oxide synthase and cyclooxygenase-2 activity by 1,2,3,4,6-penta-O-galloyl-beta-D-glucose in murine macrophage cells, Arch Pharm Res, 26, 832, 2003.
110. Park, J.W., et al., Involvement of ERK and protein tyrosine phosphatase signaling pathways in EGCG-induced cyclooxygenase-2 expression in Raw 264.7 cells, Biochem Biophys Res Commun, 286, 721, 2001.
111. Kundu, J.K., et al., Inhibition of phorbol ester-induced COX-2 expression by epigallocatechin gallate in mouse skin and cultured human mammary epithelial cells, J Nutr, 133, 3805S, 2003.
112. Li, Z.G., et al., Inhibitory effects of epigallocatechin-3-gallate on N-nitro somethylbenzylamine- induced esophageal tumorigenesis in F344 rats, Int J Oncol, 21, 1275, 2002.
113. Hwang, J.T., et al., Apoptotic effect of EGCG in HT-29 colon cancer cells via AMPK signal pathway, Cancer Lett, 2006.
114. Peng, G., et al., Green tea polyphenol (-)-epigallocatechin-3-gallate inhibits cyclooxygenase-2 expression in colon carcinogenesis, Mol Carcinog, 45, 309, 2006.
115. Shimizu, M., et al., EGCG inhibits activation of HER3 and expression of cyclooxygenase-2 in human colon cancer cells, J Exp Ther Oncol, 5, 69, 2005.
116. Chen, C., et al., Epigallocatechin-3-gallate-induced stress signals in HT-29 human colon adenocarcinoma cells, Carcinogenesis, 24, 1369, 2003.
117. Noguchi, M., et al., Inhibitory effect of the tea polyphenol, (-)-epigallocatechin gallate, on growth of cervical adenocarcinoma cell lines, Cancer Lett, 234, 135, 2006.
118. Hastak, K., et al., Role of p53 and NF-kappaB in epigallocatechin-3-gallate-induced apoptosis of LNCaP cells, Oncogene, 22, 4851, 2003.
119. Kuo, P.L. and Lin, C.C., Green tea constituent (-)-epigallocatechin-3-gallate inhibits Hep G2 cell proliferation and induces apoptosis through p53-dependent and Fas-mediated pathways, J Biomed Sci, 10, 219, 2003.
120. Ji, S.J., et al., Inhibition of proliferation and induction of apoptosis by EGCG in human osteogenic sarcoma (HOS) cells, Arch Pharm Res, 29, 363, 2006.
121. Nihal, M., et al., Anti-proliferative and proapoptotic effects of (-)-epigallocatechin-3-gallate on human melanoma: possible implications for the chemoprevention of melanoma, Int J Cancer, 114, 513, 2005.
122. Zhao, X., et al., Epigallocatechin gallate, the main ingredient of green tea induces apoptosis in breast cancer cells, Front Biosci, 11, 2428, 2006.
123. Thangapazham, R.L., et al., Green tea polyphenols and its constituent epigallocatechin gallate inhibits proliferation of human breast cancer cells in vitro and in vivo, Cancer Lett, 2006.
124. Spinella, F., et al., Antitumor effect of green tea polyphenol epigallocatechin-3- gallate in ovarian carcinoma cells: evidence for the endothelin-1 as a potential target, Exp Biol Med (Maywood), 231, 1123, 2006.
125. Qanungo, S., et al., Epigallocatechin-3-gallate induces mitochondrial membrane depolarization and caspase-dependent apoptosis in pancreatic cancer cells, Carcinogenesis, 26, 958, 2005.
126. Spinella, F., et al., Green tea polyphenol epigallocatechin-3-gallate inhibits the endothelin axis and downstream signaling pathways in ovarian carcinoma, Mol Cancer Ther, 5, 1483, 2006.
127. Suganuma, M., et al., Green tea polyphenol stimulates cancer preventive effects of celecoxib in human lung cancer cells by upregulation of GADD153 gene, Int J Cancer, 119, 33, 2006.
128. Chan, M.M., et al., Epigallocatechin-3-gallate delivers hydrogen peroxide to induce death of ovarian cancer cells and enhances their cisplatin susceptibility, J Cell Physiol, 207, 389, 2006.
129. McLaughlin, N., et al., The survivin-mediated radioresistant phenotype of glioblastomas is regulated by RhoA and inhibited by the green tea polyphenol (-)-epigallocatechin-3-gallate, Brain Res, 1071, 1, 2006.
130. Chung, J.H., et al., Dual mechanisms of green tea extract (EGCG)-induced cell survival in human epidermal keratinocytes, Faseb J, 17, 1913, 2003.
131. Oltvai, Z.N., et al., Bcl-2 heterodimerizes in vivo with a conserved homolog, Bax, that accelerates programmed cell death, Cell, 74, 609, 1993.
132. Park, H.J., et al., Epigallocatechin gallate reduces hypoxia-induced apoptosis in human hepatoma cells, Life Sci, 78, 2826, 2006.
133. Sazuka, M., et al., Interaction between the carboxyl-terminal heparin-binding domain of fibronectin and (-)-epigallocatechin gallate, Biosci Biotechnol Biochem, 62, 1031, 1998.
134. Shimizu, M., et al., EGCG inhibits activation of the insulin-like growth factor-1 receptor in human colon cancer cells, Biochem Biophys Res Commun, 334, 947, 2005.
135. Li, M., et al., Direct inhibition of insulin-like growth factor-1 receptor kinase activity by (-)-epigallocatechin-3-gallate regulates cell transformation, Cancer Epidemiol Biomarkers Prev, 16, 598, 2007.
136. Hayakawa, S., et al., Apoptosis induction by epigallocatechin gallate involves its binding to Fas, Biochem Biophys Res Commun, 285, 1102, 2001.
137. Suzuki, Y. and Isemura, M., Inhibitory effect of epigallocatechin gallate on adhesion of murine melanoma cells to laminin, Cancer Lett, 173, 15, 2001.
138. Tachibana, H., et al., A receptor for green tea polyphenol EGCG, Nat Struct Mol Biol, 11, 380, 2004.
139. Umeda, D., et al., Epigallocatechin-3-O-gallate disrupts stress fibers and the contractile ring by reducing myosin regulatory light chain phosphorylation mediated through the target molecule 67 kDa laminin receptor, Biochem Biophys Res Commun, 333, 628, 2005.
140. Ermakova, S., et al., The intermediate filament protein vimentin is a new target for epigallocatechin gallate, J Biol Chem, 280, 16882, 2005.
141. Ermakova, S., et al., EGCG overcomes resistance to etoposide-induced cell death by targeting the molecular chaperone GRP78, Cancer Res, 66, 9260, 2006.
142. Bahr, C. and Groner, B., The insulin like growth factor-1 receptor (IGF-1R) as a drug target: novel approaches to cancer therapy, Growth Horm IGF Res, 14, 287, 2004.
143. Tian, W.X., Inhibition of fatty acid synthase by polyphenols, Curr Med Chem, 13, 967, 2006.
144. Yang, C.S., et al., Tea and tea polyphenols in cancer prevention, J Nutr, 130, 472S, 2000.
145. Yang, C.S., et al., Inhibition of carcinogenesis by tea, Annu Rev Pharmacol Toxicol, 42, 25, 2002.
146. Chou, Y.H. and Goldman, R.D., Intermediate filaments on the move, J Cell Biol, 150, F101, 2000.
147. Brusselmans, K., et al., Epigallocatechin-3-gallate is a potent natural inhibitor of fatty acid synthase in intact cells and selectively induces apoptosis in prostate cancer cells, Int J Cancer, 106, 856, 2003.
148. Islam, S., et al., Involvement of caspase-3 in epigallocatechin-3-gallate-mediated apoptosis of human chondrosarcoma cells, Biochem Biophys Res Commun, 270, 793, 2000.
149. Liang, Y.C., et al., Suppression of extracellular signals and cell proliferation by the black tea polyphenol, theaflavin-3,3′-digallate, Carcinogenesis, 20, 733, 1999.
150. Kavanagh, K.T., et al., Green tea extracts decrease carcinogen-induced mammary tumor burden in rats and rate of breast cancer cell proliferation in culture, J Cell Biochem, 82, 387, 2001.
151. Kuzuhara, T., et al., DNA and RNA as new binding targets of green tea catechins, J Biol Chem, 281, 17446, 2006.
152. Chung, J.Y., et al., Mechanisms of inhibition of the Ras-MAP kinase signaling pathway in 30.7b Ras 12 cells by tea polyphenols (-)-epigallocatechin-3-gallate and theaflavin-3,3′-digallate, Faseb J, 15, 2022, 2001.
153. Pan, M.H., et al., Suppression of lipopolysaccharide-induced nuclear factor-kappaB activity by theaflavin-3,3′-digallate from black tea and other polyphenols through down-regulation of IkappaB kinase activity in macrophages, Biochem Pharmacol, 59, 357, 2000.
154. Zykova, T.A., et al., The signal transduction networks required for phosphorylation of STAT1 at Ser727 in mouse epidermal JB6 cells in the UVB response and inhibitory mechanisms of tea polyphenols, Carcinogenesis, 26, 331, 2005.
155. Sengupta, A., et al., Chemopreventive potential of diallylsulfide, lycopene and theaflavin during chemically induced colon carcinogenesis in rat colon through modulation of cyclooxygenase-2 and inducible nitric oxide synthase pathways, Eur J Cancer Prev, 15, 301, 2006.
156. Saha, P., et al., Black tea extract can modulate protein expression of H-ras, c-Myc, p53, and Bcl-2 genes during pulmonary hyperplasia, dysplasia, and carcinoma in situ, J Environ Pathol Toxicol Oncol, 24, 211, 2005.
157. Bode, A.M. and Dong, Z., The enigmatic effects of caffeine in cell cycle and cancer, Cancer Lett, 247, 26, 2007.
158. Coffee, tea, mate, methylxanthines and methylglyoxal. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. Lyon, 27 February to 6 March 1990, IARC Monogr Eval Carcinog Risks Hum, 51, 1, 1991.
159. Ito, K., et al., Caffeine induces G2/M arrest and apoptosis via a novel p53-dependent pathway in NB4 promyelocytic leukemia cells, J Cell Physiol, 196, 276, 2003.
160. He, Z., et al., Induction of apoptosis by caffeine is mediated by the p53, Bax, and caspase 3 pathways, Cancer Res, 63, 4396, 2003.
161. Lelo, A., et al., Assessment of caffeine exposure: caffeine content of beverages, caffeine intake, and plasma concentrations of methylxanthines, Clin Pharmacol Ther, 39, 54, 1986.
162. Marret, S., et al., Caffeine-induced disturbances of early neurogenesis in whole mouse embryo cultures, Brain Res, 773, 213, 1997.
163. Qi, W., et al., Caffeine induces TP53-independent G(1)-phase arrest and apoptosis in human lung tumor cells in a dose-dependent manner, Radiat Res, 157, 166, 2002.
164. Gong, J., et al., Threshold expression of cyclin E but not D type cyclins characterizes normal and tumour cells entering S phase, Cell Prolif, 28, 337, 1995.
165. Hashimoto, T., et al., Caffeine inhibits cell proliferation by G0/G1 phase arrest in JB6 cells, Cancer Res, 64, 3344, 2004.
166. Kastan, M.B., et al., Participation of p53 protein in the cellular response to DNA damage, Cancer Res, 51, 6304, 1991.
167. Kaufmann, W.K., et al., Caffeine and human DNA metabolism: the magic and the mystery, Mutat Res, 532, 85, 2003.
168. Dubrez, L., et al., Caffeine sensitizes human H358 cell line to p53-mediated apoptosis by inducing mitochondrial translocation and conformational change of Bax protein, J Biol Chem, 276, 38980, 2001.
169. Takagi, M., et al., DNA damage-associated cell cycle and cell death control is differentially modulated by caffeine in clones with p53 mutations, Leukemia, 13, 70, 1999.
170. Vavrova, J., et al., Caffeine induces a second wave of apoptosis after low dose-rate gamma radiation of HL-60 cells, Radiat Environ Biophys, 42, 193, 2003.
171. Jang, M.H., et al., Caffeine induces apoptosis in human neuroblastoma cell line SK-N-MC, J Korean Med Sci, 17, 674, 2002.
172. Essmann, F., et al., Apoptosis resistance of MCF-7 breast carcinoma cells to ionizing radiation is independent of p53 and cell cycle control but caused by the lack of caspase-3 and a caffeine-inhibitable event, Cancer Res, 64, 7065, 2004.
173. Bache, M., et al., Loss of G2/M arrest correlates with radiosensitization in two human sarcoma cell lines with mutant p53, Int J Cancer, 96, 110, 2001.
174. Minemoto, Y., et al., Characterization of adriamycin-induced G2 arrest and its abrogation by caffeine in FL-amnion cells with or without p53, Exp Cell Res, 262, 37, 2001.
175. Deplanque, G., et al., Conflicting effects of caffeine on apoptosis and clonogenic survival of human K1 thyroid carcinoma cell lines with different p53 status after exposure to cisplatin or UV irradiation, Biochem Biophys Res Commun, 314, 1100, 2004.
176. Fernandez, M.J., et al., Apoptosis induced by different doses of caffeine on Chinese hamster ovary cells, J Appl Toxicol, 23, 221, 2003.
177. Jafari, M. and Rabbani, A., Studies on the mechanism of caffeine action in alveolar macrophages: caffeine elevates cyclic adenosine monophosphate level and prostaglandin synthesis, Metabolism, 53, 687, 2004.
178. Higuchi, K., et al., Caffeine enhanced radiosensitivity of rat tumor cells with a mutant-type p53 by inducing apoptosis in a p53-independent manner, Cancer Lett, 152, 157, 2000.
179. Banin, S., et al., Enhanced phosphorylation of p53 by ATM in response to DNA damage, Science, 281, 1674, 1998.
180. Maya, R., et al., ATM-dependent phosphorylation of Mdm2 on serine 395: role in p53 activation by DNA damage, Genes Dev, 15, 1067, 2001.
181. Sarkaria, J.N., et al., Inhibition of ATM and ATR kinase activities by the radiosensitizing agent, caffeine, Cancer Res, 59, 4375, 1999.
182. Cortez, D., Caffeine inhibits checkpoint responses without inhibiting the ataxiatelangiectasia- mutated (ATM) and ATM- and Rad3-related (ATR) protein kinases, J Biol Chem, 278, 37139, 2003.
183. Block, W.D., et al., Selective inhibition of the DNA-dependent protein kinase (DNA-PK) by the radiosensitizing agent caffeine, Nucleic Acids Res, 32, 1967, 2004.
184. Deplanque, G., et al., Caffeine and the G2/M block override: a concept resulting from a misleading cell kinetic delay, independent of functional p53, Int J Cancer, 94, 363, 2001.
185. Russell, K.J., et al., Abrogation of the G2 checkpoint results in differential radiosensitization of G1 checkpoint-deficient and G1 checkpoint-competent cells, Cancer Res, 55, 1639, 1995.
186. Yao, S.L., et al., Selective radiosensitization of p53-deficient cells by caffeine-mediated activation of p34cdc2 kinase, Nat Med, 2, 1140, 1996.
187. Saito, Y., et al., Adenovirus-mediated PTEN treatment combined with caffeine produces a synergistic therapeutic effect in colorectal cancer cells, Cancer Gene Ther, 10, 803, 2003.
188. Ribeiro, J.C., et al., Caffeine-increased radiosensitivity is not dependent on a loss of G2/M arrest or apoptosis in bladder cancer cell lines, Int J Radiat Biol, 75, 481, 1999.
189. Powell, S.N., et al., Differential sensitivity of p53(-) and p53(+) cells to caffeine-induced radiosensitization and override of G2 delay, Cancer Res, 55, 1643, 1995.
190. Kitamoto, Y., et al., Caffeine diminishes cytotoxic effects of paclitaxel on a human lung adenocarcinoma cell line, Cancer Lett, 191, 101, 2003.
191. Traganos, F., et al., Caffeine modulates the effects of DNA-intercalating drugs in vitro: a flow cytometric and spectrophotometric analysis of caffeine interaction with novantrone, doxorubicin, ellipticine, and the doxorubicin analogue AD198, Cancer Res, 51, 3682, 1991.
192. Weiss, J.F. and Landauer, M.R., Protection against ionizing radiation by antioxidant nutrients and phytochemicals, Toxicology, 189, 1, 2003.
193. Surh, Y.J., et al., Molecular mechanisms underlying chemopreventive activities of anti-inflammatory phytochemicals: down-regulation of COX-2 and iNOS through suppression of NF-kappa B activation, Mutat Res, 480-481, 243, 2001.
194. Kaul, P.N. and Joshi, B.S., Alternative medicine: herbal drugs and their critical appraisal-part II, Prog Drug Res, 57, 1, 2001.
195. Wilkinson, J.M., What do we know about herbal morning sickness treatments? A literature survey, Midwifery, 16, 224, 2000.
196. Wilkinson, J.M., Effect of ginger tea on the fetal development of Sprague-Dawley rats, Reprod Toxicol, 14, 507, 2000.
197. Ginger for nausea, Harvard Women’s Health Watch, 7, 7, 1999.
198. Afzal, M., et al., Ginger: an ethnomedical, chemical and pharmacological review, Drug Metabol Drug Interact, 18, 159, 2001.
199. Grant, K.L. and Lutz, R.B., Ginger, Am J Health Syst Pharm, 57, 945, 2000.
200. Langner, E., et al., Ginger: history and use, Adv Ther, 15, 25, 1998.
201. Surh, Y.J., et al., Chemoprotective properties of some pungent ingredients present in red pepper and ginger, Mutat Res, 402, 259, 1998.
202. Lee, E., et al., Suppression of mouse skin tumor promotion and induction of apoptosis in HL-60 cells by Alpinia oxyphylla Miquel (Zingiberaceae), Carcinogenesis, 19, 1377, 1998.
203. Lee, E. and Surh, Y.J., Induction of apoptosis in HL-60 cells by pungent vanilloids, [6]-gingerol and [6]-paradol, Cancer Lett, 134, 163, 1998.
204. Bode, A.M., et al., Inhibition of epidermal growth factor-induced cell transformation and activator protein 1 activation by [6]-gingerol, Cancer Res, 61, 850, 2001.
205. Surh, Y.J., Anti-tumor promoting potential of selected spice ingredients with antioxidative and anti-inflammatory activities: a short review, Food Chem Toxicol, 40, 1091, 2002.
206. Bode, A.M. and Dong, Z., Ginger, in Herbal and Traditional Medicine: Molecular Aspects of Health, L. Packer, C.N. Ong, and B. Halliwell, Eds., Marcel Dekker, New York, 2004, 165.
207. Ahmad, N., et al., Antioxidants in chemoprevention of skin cancer, Curr Probl Dermatol, 29, 128, 2001.
208. Aeschbach, R., et al., Antioxidant actions of thymol, carvacrol, 6-gingerol, zingerone and hydroxytyrosol, Food Chem Toxicol, 32, 31, 1994.
209. Halvorsen, B.L., et al., A systematic screening of total antioxidants in dietary plants, J Nutr, 132, 461, 2002.
210. Shobana, S. and Naidu, K.A., Antioxidant activity of selected Indian spices, Prostaglandins Leukot Essent Fatty Acids, 62, 107, 2000.
211. Reddy, A.C. and Lokesh, B.R., Studies on spice principles as antioxidants in the inhibition of lipid peroxidation of rat liver microsomes, Mol Cell Biochem, 111, 117, 1992.
212. Krishnakantha, T.P. and Lokesh, B.R., Scavenging of superoxide anions by spice principles, Indian J Biochem Biophys, 30, 133, 1993.
213. Kim, H.W., et al., Screening of edible Japanese plants for suppressive effects on phorbol ester-induced superoxide generation in differentiated HL-60 cells and AS52 cells, Cancer Lett, 176, 7, 2002.
214. Topic, B., et al., Enhanced maze performance and reduced oxidative stress by combined extracts of Zingiber officinale and Ginkgo biloba in the aged rat, Neurobiol Aging, 23, 135, 2002.
215. Ahmed, R.S., et al., Influence of dietary ginger (Zingiber officinale Rosc.) on oxidative stress induced by malathion in rats, Food Chem Toxicol, 38, 443, 2000.
216. Ahmed, R.S., et al., Influence of dietary ginger (Zingiber officinale Rosc.) on antioxidant defense system in rat: comparison with ascorbic acid, Indian J Exp Biol, 38, 604, 2000.
217. Ippoushi, K., et al., [6]-Gingerol inhibits nitric oxide synthesis in activated J774.1 mouse macrophages and prevents peroxynitrite-induced oxidation and nitration reactions, Life Sci, 73, 3427, 2003.
218. Imanishi, N., et al., Inducible activity of ginger rhizome (Zingiber offifinale Rosc.) on the mRNA expression of macrophage-inducible nitric oxide (NO) synthase and NO production in a macrophage cell line, RAW264.7 cells, Am J Chin Med, 32, 727, 2004.
219. Nakamura, Y., et al., Zerumbone, a tropical ginger sesquiterpene, activates phase II drug metabolizing enzymes, FEBS Lett, 572, 245, 2004.
220. Jagetia, G.C., et al., Influence of ginger rhizome (Zingiber officinale Rosc) on survival, glutathione and lipid peroxidation in mice after whole-body exposure to gamma radiation, Radiat Res, 160, 584, 2003.
221. Jagetia, G., et al., Ginger (Zingiber officinale Rosc.), a dietary supplement, protects mice against radiation-induced lethality: mechanism of action, Cancer Biother Radiopharm, 19, 422, 2004.
222. Vimala, S., et al., Anti-tumour promoter activity in Malaysian ginger rhizobia used in traditional medicine, Br J Cancer, 80, 110, 1999.
223. Kapadia, G.J., et al., Inhibitory effect of herbal remedies on 12-O-tetradecanoylphorbol-13-acetate-promoted Epstein-Barr virus early antigen activation, Pharmacol Res, 45, 213, 2002.
224. Katiyar, S.K., et al., Inhibition of tumor promotion in SENCAR mouse skin by ethanol extract of Zingiber officinale rhizome, Cancer Res, 56, 1023, 1996.
225. Park, K.K., et al., Inhibitory effects of [6]-gingerol, a major pungent principle of ginger, on phorbol ester-induced inflammation, epidermal ornithine decarboxylase activity and skin tumor promotion in ICR mice, Cancer Lett, 129, 139, 1998.
226. Chung, W.Y., et al., Antioxidative and antitumor promoting effects of [6]-paradol and its homologs, Mutat Res, 496, 199, 2001.
227. Kim, H.W., et al., Suppressive effects of mioga ginger and ginger constituents on reactive oxygen and nitrogen species generation, and the expression of inducible pro-inflammatory genes in macrophages, Antioxid Redox Signal, 7, 1621, 2005.
228. Yoshimi, N., et al., Modifying effects of fungal and herb metabolites on azoxymethaneinduced intestinal carcinogenesis in rats, Jpn J Cancer Res, 83, 1273, 1992.
229. Mahady, G.B., et al., Ginger (Zingiber officinale Rosc.) and the gingerols inhibit the growth of Cag A+ strains of Helicobacter pylori, Anticancer Res, 23, 3699, 2003.
230. Manju, V. and Nalini, N., Chemopreventive efficacy of ginger, a naturally occurring anticarcinogen during the initiation, post-initiation stages of 1,2 dimethylhydrazineinduced colon cancer, Clin Chim Acta, 358, 60, 2005.
231. Murakami, A., et al., Zerumbone, a sesquiterpene in subtropical ginger, suppresses skin tumor initiation and promotion stages in ICR mice, Int J Cancer, 110, 481, 2004.
232. Dias, M.C., et al., Lack of chemopreventive effects of ginger on colon carcinogenesis induced by 1,2-dimethylhydrazine in rats, Food Chem Toxicol, 44, 877, 2006.
233. Thatte, U., et al., Modulation of programmed cell death by medicinal plants, Cell Mol Biol (Noisy-le-grand), 46, 199, 2000.
234. Wang, C.C., et al., Effects of 6-gingerol, an antioxidant from ginger, on inducing apoptosis in human leukemic HL-60 cells, In Vivo, 17, 641, 2003.
235. Hsu, M.H., et al., 1-(3,4-dimethoxyphenyl)-3,5-dodecenedione (I6) induces G1 arrest and apoptosis in human promyelocytic leukemia HL-60 cells, Leuk Res, 29, 1399, 2005.
236. Keum, Y.S., et al., Induction of apoptosis and caspase-3 activation by chemopreventive [6]-paradol and structurally related compounds in KB cells, Cancer Lett, 177, 41, 2002.
237. Miyoshi, N., et al., Dietary ginger constituents, galanals A and B, are potent apoptosis inducers in Human T lymphoma Jurkat cells, Cancer Lett, 199, 113, 2003.
238. Koo, K.L., et al., Gingerols and related analogues inhibit arachidonic acid-induced human platelet serotonin release and aggregation, Thromb Res, 103, 387, 2001.
239. Tjendraputra, E., et al., Effect of ginger constituents and synthetic analogues on cyclooxygenase-2 enzyme in intact cells, Bioorg Chem, 29, 156, 2001.
240. Kim, S.O., et al., Inhibitory effects of [6]-gingerol on PMA-induced COX-2 expression and activation of NF-kappaB and p38 MAPK in mouse skin, Biofactors, 21, 27, 2004.
241. Dean, J.L., et al., p38 mitogen-activated protein kinase regulates cyclooxygenase-2 mRNA stability and transcription in lipopolysaccharide-treated human monocytes, J Biol Chem, 274, 264, 1999.
242. Kim, S.O., et al., [6]-Gingerol inhibits COX-2 expression by blocking the activation of p38 MAP kinase and NF-kappaB in phorbol ester-stimulated mouse skin, Oncogene, 24, 2558, 2005.
243. Kiuchi, F., et al., Inhibition of prostaglandin and leukotriene biosynthesis by gingerols and diarylheptanoids, Chem Pharm Bull (Tokyo), 40, 387, 1992.
244. Takada, Y., et al., Zerumbone abolishes NF-kappaB and IkappaBalpha kinase activation leading to suppression of antiapoptotic and metastatic gene expression, upregulation of apoptosis, and downregulation of invasion, Oncogene, 24, 6957, 2005.
245. Kim, E.C., et al., [6]-Gingerol, a pungent ingredient of ginger, inhibits angiogenesis in vitro and in vivo, Biochem Biophys Res Commun, 335, 300, 2005.