Abstract
Green tea is now an acknowledged cancer preventive in Japan. Based on evidence that colorectal adenomas and prostate cancer in humans have been prevented, we review here the concept that the combination of anticancer drugs with green tea catechin synergistically induces apoptosis of human cancer cells, inhibits tumor formation in mice, and enhances inhibition of tumor growth in xenograft mouse models. As a molecular mechanism by the combination, the induction of growth arrest and DNA damage-inducible 153 (GADD153, CHOP) gene expression is discussed in relation to death receptor 5 and TRAIL-apoptotic pathway. The combination of anticancer drugs with green tea could be a new cancer therapeutic strategy in humans.
Copyright © 2012 Elsevier Ireland Ltd. All rights reserved.
MeSH terms
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Animals
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Antineoplastic Agents, Phytogenic / pharmacology*
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Antineoplastic Combined Chemotherapy Protocols / pharmacology*
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Apoptosis / drug effects
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Catechin / analogs & derivatives
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Catechin / pharmacology
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Cell Line, Tumor
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Drug Synergism
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Gene Expression Regulation, Neoplastic / drug effects
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Humans
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Mice
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Neoplasms / drug therapy*
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Neoplasms / genetics
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Neoplasms / metabolism
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Neoplasms / pathology
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Receptors, TNF-Related Apoptosis-Inducing Ligand / metabolism
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TNF-Related Apoptosis-Inducing Ligand / metabolism
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Tea*
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Transcription Factor CHOP / genetics
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Transcription Factor CHOP / metabolism
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Tumor Burden / drug effects
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Xenograft Model Antitumor Assays
Substances
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Antineoplastic Agents, Phytogenic
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DDIT3 protein, human
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Receptors, TNF-Related Apoptosis-Inducing Ligand
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TNF-Related Apoptosis-Inducing Ligand
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TNFSF10 protein, human
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Tea
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Transcription Factor CHOP
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Catechin
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epigallocatechin gallate