Background: Epidemiological analysis demonstrated that there are negative correlation between green tea consumption and the risk of non-Hodgkin lymphoma and prostate cancer. Recent studies show (–)-epigallocatechin-3-O-gallate (EGCG), or major green tea polyphenol, suppresses the proliferation of cancer cells and induces cell death without adversely affecting normal cells. As a result, several molecular mechanisms have been suggested to be responsible for this effect. For example, 67-kDa laminin receptor (67LR) was recently identified as the sensing molecule for EGCG. 67LR overexpresses in cancer cells and plays a crucial role in the selective toxicity of EGCG. Moreover, possible downstream mechanisms were suggested in 67LR-dependent the anti-cancer effect of EGCG. This review focused on the molecular mechanism of EGCG and developing a novel strategy to amplify its effect.
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