Chemopreventive effects of dietary phytochemicals against cancer invasion and metastasis: phenolic acids, monophenol, polyphenol, and their derivatives |
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Authors: | Weng Chia-Jui Yen Gow-Chin |
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Affiliation: | a Graduate Institute of Applied Science of Living, Tainan University of Technology, 529 Zhongzheng Rd., Yongkang District, Tainan City 71002, Taiwan b Department of Food Science and Biotechnology, National Chung Hsing University, 250 Kuokuang Road, Taichung 40227, Taiwan |
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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. |
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Keywords: | 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&prime -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 |
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