Abstract
Cancer metastasis is the major cause of cancer-related death, and chemoprevention
is defined as the use of natural or synthetic substances to prevent cancer formation
or cancer progress. Evidence that phenolic compounds may have a potential inhibitory
effect on cancer invasion and metastasis is increasingly being reported in the scientific
literature. Curcumin, resveratrol, and their related derivatives are the most studied
compounds in this topic so far; gallic acid, chlorogenic acid, caffeic acid, carnosol,
capsaicin, 6-shogaol, 6-gingerol, and their corresponding derivatives are also suggested
to be the active members of the phenolic family on anti-invasion and anti-metastasis.
Because metastasis occurs through a multistep process, these bioactives might act
on a variety of stages of the metastatic process to prevent tumor cells from metastasizing.
This review summarizes the common protein targets and signaling pathways for the inhibition
of invasion and metastasis as well as past publications on the in vitro and in vivo effects and molecular mechanisms of phenolic acids, monophenol, polyphenol, and their
derivatives, except flavonoids, on cancer invasion and metastasis. Based on these
data, we conclude that the daily consumption of natural dietary components that are
rich in phenolics could be beneficial for the prevention of cancer metastasis.
Abbreviations:
Akt (protein kinase B), AP-1 (activator protein-1), BDMC (bisdemethoxycurcumin), CDCQ (3-caffeoyl,4-dihydrocaffeoylquinic acid), CGA (chlorogenic acid), DMC (demethoxycurcumin), ECM (extracellular matrix), EGF (epidermal growth factor), EMT (epithelial–mesenchymal transition), ERK (extracellular signal-regulated kinase), FAK (focal adhesion kinase), FGF (fibroblast growth factor), GA (gallic acid), HGF (hepatocyte growth factor), HIF (hypoxia-inducible factors), ICAM (intercellular adhesion molecule), IKK (IkBα kinase), JNK (c-Jun N-terminal kinase), MAPK (mitogen activated protein kinase), MMP (matrix metalloproteinase), MR-3 (3,5,4′-trimethoxy-trans-stilbene), MT-1 MMP (membrane type-1 MMP), NF-κB (nuclear factor-kappaB), p38/MAPK (p38 mitogen-activated protein kinase), PAI (plasminogen activator inhibitor), PI3K (phosphoinositide-3 kinase), PKC (protein kinase C), PMA (phorbol-12-myristate-13-acetate), ROS (reactive oxygen species), TGFβ (transforming growth factor β), TIMP (tissue inhibitor metalloproteinase protein), TNF (tumor necrosis factor), uPA (urokinase plasminogen activator)Keywords
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Article Info
Publication History
Published online: April 13, 2011
Accepted:
March 13,
2011
Received in revised form:
March 3,
2011
Received:
October 2,
2010
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© 2011 Elsevier Ltd. Published by Elsevier Inc. All rights reserved.
