Molecular mechanisms explaining the preventive effects of catechins on the development of proliferative diseases.
Various growth factors such as the platelet derived growth factor (PDGF), insulin-like growth factor (IGF), epidermal growth factor (EGF), fibroblast growth factor (FGF), and vascular endothelial growth factor (VEGF) transduce their mitogenic signals through the activation of tyrosine kinase receptors (RTKs). Since enhanced RTK activity has been associated with the development of proliferative diseases such as atherosclerosis and cancer, there has been an increased interest recently in the development of small molecule RTK inhibitors for the prevention/treatment of the aforementioned diseases. Many cell culture and animal studies have shown that catechins, the main compounds of the green tea leaves, are potent natural inhibitors of several RTKs. In the present article we review the various molecular and cellular mechanisms through which catechins inhibit the growth factor-RTK-mediated signal transduction pathways and exert their antiproliferative/apoptotic effects.
Gouni-Berthold
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Second Department of Internal Medicine, University of Cologne, 50924 Cologne, Germany.
Sachinidis
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A
D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D028241:Camellia sinensis / Q000737:chemistry; D002392:Catechin / Q000494:pharmacology*; D003324:Coronary Artery Disease / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D006133:Growth Substances / Q000502:physiology; D006801:Humans; D009369:Neoplasms / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D009389:Neovascularization, Pathologic / Q000378:metabolism / Q000517:prevention & control; D017382:Reactive Oxygen Species / Q000378:metabolism; D020794:Receptor Protein-Tyrosine Kinases / Q000037:antagonists & inhibitors*; D015398:Signal Transduction; D013662:Tea / Q000737:chemistry
D006133:Growth Substances; D017382:Reactive Oxygen Species; D013662:Tea; D002392:Catechin; D020794:Receptor Protein-Tyrosine Kinases