To determine the anticancer potential of various green tea catechins, their tumor-suppressive and/or apoptotic effects must be differentiated across a spectrum of human malignancies. This in vitro study tested the hypothesis that growth suppression by epicatechin (EC), epigallocatechin (EGC), EC 3-gallate (ECG), and EGC 3-gallate (EGCG) differs with cancer type. Cell lines developed from organ-confined (HH870) and metastatic (DU145) prostate cancer (CaP), from moderately differentiated (HH450) and poorly differentiated (HH639) epithelial ovarian cancer (EOC), and from melanoma (CII-0356) were grown with or without EC, EGC, ECG, or EGCG. When untreated cells reached confluency, viability and doubling time were measured for treated and untreated cells. Dosimetry and 50% inhibition of proliferation (IC50) were measured. EC had no effect on any cell line except HH639 EOC. EGC had no effect on CaP and EOC cells but significantly inhibited growth of melanoma cells. ECG was the most potent inhibitor of growth and cell cycle of CaP and EOC cells. ECG and/or EGCG prolonged the doubling time of DU145 CaP and both EOC lines; in fact, ECG totally arrested doubling of HH639 cells: the cell number declined, possibly reflecting cell death. IC50 values for CaP cells were 24 to 30 μM with ECG, versus 42 to 89 μM with EGCG. ECG inhibited DU145, HH870, HH450 and HH639 cells at concentrations of 24, 27, 29 and 30 μM, respectively, whereas EGCG inhibited DU145, HH870, HH450 and HH639 cells at concentrations of 89, 45, 62 and 42 μM, respectively. EGCG at 25 μM significantly (p>0.05) enhanced proliferation of CaP cell lines but not EOC lines. Unlike the gender-based cancer cells, melanoma cells were significantly inhibited by EGC; EGCG and ECG had progressively lesser effects on melanoma cell proliferation. In the gender-based cancer cells, ECG was a more potent growth suppressor than EGCG.

[Proc Amer Assoc Cancer Res, Volume 47, 2006]