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Nutrition, Diet and Cancer pp 339–376Cite as

Intracellular Signaling Network as a Prime Chemotherapy Target of Green Tea Catechin, (–)-Epigallocatechin-3-gallate

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Abstract

Chemoprevention is an attempt to use either naturally occurring or synthetic substances or their mixtures to intervene in the progress of carcinogenesis. Recently, it has been shown that green tea phytochemicals alter gene expression, directly or indirectly, thereby regulating the carcinogenic processes. Epigallocatechin-3-gallate (EGCG), the major antioxidant polyphenolic compound present in green tea, is a promising chemopreventive agent. EGCG has been shown to exert growth-inhibitory potential of various cancer cells in culture and antitumor activity in vivo models. EGCG could interact with various molecules like proteins, transcription factors, and enzymes, which block multiple stages of carcinogenesis. Moreover, much of the cancer chemopreventive effects of EGCG that regulates cell proliferation and apoptosis effects by altering the expression of cell cycle regulatory proteins, activating killer caspases, induction of phase II enzymes, mediation of anti-oxidative, anti-inflammation responses, and suppressing oncogenic transcription factors and pluripotency maintain factors. In vitro and in vivo studies have demonstrated that EGCG blocks carcinogenesis by affecting a wide array of signal transduction pathways involved in cell proliferation, transformation, inflammation, apoptosis, metastasis and invasion. EGCG stimulates telomere fragmentation through inhibiting telomerase activity. Recent reports demonstrated that EGCG inhibits DNA methyltransferases, proteases, and dihydrofolate reductase activities, which would affect transcription of tumor suppressor genes and protein synthesis. To develop EGCG as an anticarcinogenic agent, more clear understanding of the cell signaling pathways and the molecular targets responsible for chemopreventive and chemotherapeutic effects are needed. This review summarizes recent preclinical and clinical research on the EGCG-induced cellular signal transduction events which implicate in prevention and therapy of cancer.

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Abbreviations

α-TNF:

Alpha-tumor necrosis factor

AMPK:

Adenosine monophosphate-activated protein kinase

AP1:

Activator protein 1

AREs:

Antioxidant responsive elements

Bcl-2:

B-cell lymphoma-2

CAT:

Catalase

CDKN2A:

Cyclin dependent kinase 2A

Cdks:

Cyclin-dependent kinases

c-IAP1:

Cellular inhibitor of apoptosis protein1

COX-2:

Cyclooxygenase-2

CpG:

Cytosine-phosphate-guanine

CSCs:

Cancer stem cells

CYP:

Cytochrome P450

DHFR:

Dihydrofolate reductase

DIABLO:

Direct inhibitor of apoptosis-binding protein with low pI

DNMTs:

DNA methyltransferases

EGCG:

(-)-Epigallocatechin-3-gallate

EGFR:

Epidermal growth factor receptor

EpRE:

Electrophile-responsive element

ERK:

Extracellular signal-regulated kinase

FAK:

Focal adhesion kinase

FKHR:

Forkhead homolog of rhabdosarcoma

GFRs:

Growth factor receptors

GPx:

Glutathione peroxidase

GR:

Glutathione reductase

GST:

Glutathione S-transferase

H2O2 :

Hydrogen peroxide

HATs:

Histone acetyl transferases

HDACs:

Histone deacetylases

HER:

Human epidermal receptor

HIF:

Hypoxia inducible factor

hTERT:

human telomerase reverse transcriptase

HUVEC:

Human vascular endothelial cell

IKK:

I kappa B kinase

IL-1:

Interleukin 1

JNK:

Jun NH2-terminal kinase

LPs:

Lipopolysaccharides

MAP:

Mitogen-activated protein

MBD:

Methyl-CpG binding domain

Mcl-1:

Myeloid cell leukemia 1

mdm2:

mouse double minute 2

MEKK1:

Mitogen-activated protein/ERK kinase 1

MLH1:

MutL homologue 1

MMPs:

Matrix metalloproteinases

MRLC:

Myosin regulatory light chain

MT1-MMP:

Membrane Type 1-matrix metalloproteinase

NFκB:

Nuclear factor kappaB

NQO:

NADPH quinone oxidoreductase

Nrf:

NF-E2 p45-related factor

O •−2 :

Superoxide anion radical

•OH:

Hydroxyl radical

p90RSK:

90 kDa ribosomal S6 kinase

PCNA:

Proliferating cell nuclear antigen

PDGF:

Platelet-derived growth factor

PGE2:

Prostaglandins E2

PI3K:

Phosphatidylinositol- 3-kinase

PKA:

Protein kinase A

PPAR:

Peroxisome proliferator-activated receptor

pRb:

Retinoblastoma protein

PUMA:

P53 upregulated modulator of apoptosis

RAR:

Retinoic acid receptor

RECK:

Reversion-inducing cysteine-rich protein with Kazal motifs

RTK:

Receptor tyrosine kinase

RXRα:

Retinoid X receptor alpha

SAM:

S-adenosyl-methionine

siRNA:

Small-interfering RNA

Smac:

Second mitochondria-derived activator of caspase

SOD:

Superoxide dismutase

STAT:

Signal transducers and activators of transcription

TERT:

Telomerase reverse transcriptase

TIMP:

Tissue inhibitor of metalloproteinase

TRAIL:

Tumor necrosis factor-related apoptosis-inducing ligand

TRAMP:

Transgenic adenocarcinoma of the mouse prostate

TSGs:

Tumor suppressor genes

uPA:

Urokinase plasminogen activator

VEGF:

Vascular endothelial growth factor

XIAP:

X-linked inhibitor of apoptosis protein

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Acknowledgements

We thank our lab members for critical reading of the manuscript. This work was supported in part by the grants from the National Institutes of Health (R01CA125262, RO1CA114469 and RO1CA125262-02S1) and Kansas Bioscience Authority.

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  1. Department of Pharmacology, Toxicology and Therapeutics, and Medicine, The University of Kansas Cancer Center, The University of Kansas Medical Center, 3901 Rainbow Boulevard, Kansas City, KS, 66160, USA

    Brahma N. Singh & Rakesh K. Srivastava

  2. Department of Pathology and Laboratory Medicine, The University of Kansas Cancer Center, The University of Kansas Medical Center, 3901 Rainbow Boulevard, Kansas City, KS, 66160, USA

    Sharmila Shankar

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  1. Brahma N. Singh
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Correspondence to Rakesh K. Srivastava .

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  1. , Pathology and Laboratory Medicine, University of Kansas Medical Center, Rainbow Blvd 3901, Kansas City, 66160, Kansas, USA

    Sharmila Shankar

  2. , Pharmacology and Toxicology, University of Kansas Medical Center, Rainbow Blvd 3901, Kansas City, 66160, Kansas, USA

    Rakesh K. Srivastava

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Singh, B.N., Shankar, S., Srivastava, R.K. (2012). Intracellular Signaling Network as a Prime Chemotherapy Target of Green Tea Catechin, (–)-Epigallocatechin-3-gallate. In: Shankar, S., Srivastava, R. (eds) Nutrition, Diet and Cancer. Springer, Dordrecht. https://doi.org/10.1007/978-94-007-2923-0_15

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