Cancer and Metastasis Reviews

, Volume 33, Issue 1, pp 41–85

Dietary phytochemicals alter epigenetic events and signaling pathways for inhibition of metastasis cascade

Phytoblockers of metastasis cascade

Authors

  • B. N. Singh
    • Research and Development DivisionSowbhagya Biotech Private Limited
  • Harikesh Bahadur Singh
    • Department of Mycology & Plant Pathology, Institute of Agricultural SciencesBanaras Hindu University
  • A. Singh
    • Department of Mycology & Plant Pathology, Institute of Agricultural SciencesBanaras Hindu University
  • Alim H. Naqvi
    • Centre of Excellence in Materials Science (Nanomaterials), Department of Applied Physics, Z.H. College of Engineering & TechnologyAligarh Muslim University
    • Centre of Excellence in Materials Science (Nanomaterials), Department of Applied Physics, Z.H. College of Engineering & TechnologyAligarh Muslim University
NON-THEMATIC REVIEW

DOI: 10.1007/s10555-013-9457-1

Cite this article as:
Singh, B.N., Singh, H.B., Singh, A. et al. Cancer Metastasis Rev (2014) 33: 41. doi:10.1007/s10555-013-9457-1

Abstract

Cancer metastasis is a multistep process in which a cancer cell spreads from the site of the primary lesion, passes through the circulatory system, and establishes a secondary tumor at a new nonadjacent organ or part. Inhibition of cancer progression by dietary phytochemicals (DPs) offers significant promise for reducing the incidence and mortality of cancer. Consumption of DPs in the diet has been linked to a decrease in the rate of metastatic cancer in a number of preclinical animal models and human epidemiological studies. DPs have been reported to modulate the numerous biological events including epigenetic events (noncoding micro-RNAs, histone modification, and DNA methylation) and multiple signaling transduction pathways (Wnt/β-catenin, Notch, Sonic hedgehog, COX-2, EGFR, MAPK-ERK, JAK-STAT, Akt/PI3K/mTOR, NF-κB, AP-1, etc.), which can play a key role in regulation of metastasis cascade. Extensive studies have also been performed to determine the molecular mechanisms underlying antimetastatic activity of DPs, with results indicating that these DPs have significant inhibitory activity at nearly every step of the metastatic cascade. DPs have anticancer effects by inducing apoptosis and by inhibiting cell growth, migration, invasion, and angiogenesis. Growing evidence has also shown that these natural agents potentiate the efficacy of chemotherapy and radiotherapy through the regulation of multiple signaling pathways. In this review, we discuss the variety of molecular mechanisms by which DPs regulate metastatic cascade and highlight the potentials of these DPs as promising therapeutic inhibitors of cancer.

Keywords

Dietary phytochemicalsMicro-RNAsEpigenetic modificationsSignaling pathwaysCancerMetastasisCombine therapyNanochemoprevention

Abbreviations

ABCG2

ATP-binding cassette sub-family G member 2

ACSL1

Acyl-CoA synthetase long-chain family member 1

AKBA

Acetyl-11-keto-β-boswellic acid

ALDH

Aldehyde dehydrogenase

AP-1

Activator protein-1

APC

Adenomatous polyposis coli

BAFF

B cell activating factor of the TNF family

Bcl-2

B cell lymphoma-2

BTG3

B cell translocation gene 3

CCND2

Cyclin D2

Cdk

Cyclin-dependent kinase

COX-2

Cyclooxygenase-2

CSCs

Cancer stem cells

DNMT

DNA methyltransferase

DRs

Death receptors

EGCG

Epigallocatechin-3-gallate

EMT

Epithelial–mesenchymal transition

ERK

Extracellular signal-regulated kinase

FOXO

Forkhead box O

GSK3β

Glycogen synthase kinase 3 beta

GSTP1

Glutathione S-transferase pi 1

GTPs

Green tea polyphenols

HAT

Histone acetyltransferase

HDAC

Histone deacetyltransferase

HER2

Human epidermal growth factor receptor 2

Hh

Sonic hedgehog

hMLH1

Human mutL homologue 1

hTERT

Human telomerase reverse transcriptase

I3C

Indole-3-carbinol

ICAM-1

Intercellular adhesion molecule-1

IkBα

Inhibitory kappa B alpha

IKK

IkBα kinase

IL

Interleukin

iNOS

Inducible nitric oxide synthase

IRAK-1

IL-1 receptor-associated kinase 1

JAK/STAT

Janus kinase/signal transducers and activators of transcription

JNK

c Jun N-terminal kinase

LDH

Lactate dehydrogenase

LOX

Lipoxygenase

LPS

Lipopolysaccharide

MAPK

Mitogen-activated protein kinases

MBD2

Methyl-CpG binding domain protein 2

MGMT

Methyl guanine methyl transferase

miRs

Micro-RNAs

MMP

Matrix metalloproteinase

MTA-2

Metastasis-associated protein 2

mTOR

Mammalian target of rapamycin

NF-AT

Nuclear factor of activated T cells

NF-κB

Nuclear factor-kappa B

NIK

NF-κB-inducing kinase

PARP

Polyadenosine-5′-diphosphate-ribose polymerase

PDGF

Platelet-derived growth factor

PDK

Pyruvate dehydrogenase kinase

PGE2

Prostaglandin E2

PI3K

Phosphoinositide 3-kinase

PITCH

Phenyl isothiocyanate

PTEN

Phosphatase and tensin homolog

RARβ

Retinoic acid receptor β

SFN

Sulforaphane

TGF

Transforming growth factor

TNF

Tumor necrosis factor

TPA

Phorbol 12-O-tetradecanoate-13-acetate

TRAMP

Transgenic adenocarcinoma of mouse prostate

TSGs

Tumor suppressor genes

UVB

Ultraviolet B

VEGF

Vascular endothelial growth factor

ZEB1

Zinc finger E-box binding homeobox 1

Copyright information

© Springer Science+Business Media New York 2014