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Nutrients 2018, 10(12), 1936; https://doi.org/10.3390/nu10121936

Molecular Targets of Epigallocatechin—Gallate (EGCG): A Special Focus on Signal Transduction and Cancer

1,†
,
1,2,†,* , 1,2,3
and
1,2,3
1
Department of Medicine and Surgery, University of Parma, Via Gramsci 14, 43126 Parma, Italy
2
National Institute of Biostructure and Biosystems (INBB), Viale Medaglie d’Oro 305, 00136 Rome, Italy
3
Centre for Molecular and Translational Oncology (COMT), University of Parma, Parco Area delle Scienze 11/a, 43124 Parma, Italy
These authors contributed equally to this work.
*
Author to whom correspondence should be addressed.
Received: 7 November 2018 / Revised: 30 November 2018 / Accepted: 4 December 2018 / Published: 6 December 2018
(This article belongs to the Special Issue Tea in Health and Disease)
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Abstract

Green tea is a beverage that is widely consumed worldwide and is believed to exert effects on different diseases, including cancer. The major components of green tea are catechins, a family of polyphenols. Among them, epigallocatechin-gallate (EGCG) is the most abundant and biologically active. EGCG is widely studied for its anti-cancer properties. However, the cellular and molecular mechanisms explaining its action have not been completely understood, yet. EGCG is effective in vivo at micromolar concentrations, suggesting that its action is mediated by interaction with specific targets that are involved in the regulation of crucial steps of cell proliferation, survival, and metastatic spread. Recently, several proteins have been identified as EGCG direct interactors. Among them, the trans-membrane receptor 67LR has been identified as a high affinity EGCG receptor. 67LR is a master regulator of many pathways affecting cell proliferation or apoptosis, also regulating cancer stem cells (CSCs) activity. EGCG was also found to be interacting directly with Pin1, TGFR-II, and metalloproteinases (MMPs) (mainly MMP2 and MMP9), which respectively regulate EGCG-dependent inhibition of NF-kB, epithelial-mesenchimal transaction (EMT) and cellular invasion. EGCG interacts with DNA methyltransferases (DNMTs) and histone deacetylases (HDACs), which modulates epigenetic changes. The bulk of this novel knowledge provides information about the mechanisms of action of EGCG and may explain its onco-suppressive function. The identification of crucial signalling pathways that are related to cancer onset and progression whose master regulators interacts with EGCG may disclose intriguing pharmacological targets, and eventually lead to novel combined treatments in which EGCG acts synergistically with known drugs. View Full-Text
Keywords: green tea catechins; epigallocatechin-gallate (EGCG); 67LR; cancer apoptosis; cell death; chemoprevention; gene expression green tea catechins; epigallocatechin-gallate (EGCG); 67LR; cancer apoptosis; cell death; chemoprevention; gene expression
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Negri, A.; Naponelli, V.; Rizzi, F.; Bettuzzi, S. Molecular Targets of Epigallocatechin—Gallate (EGCG): A Special Focus on Signal Transduction and Cancer. Nutrients 2018, 10, 1936.

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