Abstract
The inhibitory activities of tea catechins against carcinogenesis and cancer cell growth have been demonstrated in a large number of laboratory studies. Many mechanisms for modulating cancer signaling and metabolic pathways have been proposed based on numerous studies in cell lines with (-)-epigallocatechin-3-gallate, the most abundant and active tea catechin. Nevertheless, the molecular basis for the proposed mechanisms and whether these mechanisms indeed contribute to the anticancer activities in vivo are not clearly known. This chapter reviews the basic redox properties of tea catechins, their binding to key enzymes and signal transduction proteins, and other mechanisms that lead to suppression of cell proliferation, increased apoptosis, and inhibition of angiogenesis. More weight is put on studies in vivo over experiments in vitro. It also discusses key issues involved in extrapolating results from cell line studies to mechanistic insights in vivo.