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Objective: To evaluate effects of epigallocatechin-3-gallate (EGCG) on the viability, membrane properties, and zinc distribution, with and without the presence of Zn(2+), in human prostate carcinoma LNCaP cells., Methods: We examined changes in cellular morphology and membrane fluidity of LNCaP cells, distribution of cellular zinc, and the incorporated portion of EGCG after treatments with EGCG, Zn(2+), and EGCG+Zn(2+)., Results: We observed an alteration in cellular morphology and a decrease in membrane fluidity of LNCaP cells after treatment with EGCG or Zn(2+). The proportion of EGCG incorporated into liposomes treated with the mixture of EGCG and Zn(2+) at the ratio of 1:1 was 90.57%, which was significantly higher than that treated with EGCG alone (30.33%). Electron spin resonance (ESR) studies and determination of fatty acids showed that the effects of EGCG on the membrane fluidity of LNCaP were decreased by Zn(2+). EGCG accelerated the accumulation of zinc in the mitochondria and cytosol as observed by atomic absorption spectrometer., Conclusion: These results show that EGCG interacted with cell membrane, decreased the membrane fluidity of LNCaP cells, and accelerated zinc accumulation in the mitochondria and cytosol, which could be the mechanism by which EGCG inhibits proliferation of LNCaP cells. In addition, high concentrations of Zn(2+) could attenuate the actions elicited by EGCG.

In this paper, the cytotoxicity of EGCG against PC-3 prostate cancer cells and its molecular mechanism in the presence and absence of Zn2+ in vitro were investigated. The results showed that both EGCG and Zn2+ suppressed clonegenecity of PC-3 cells, and the suppression effect was enhanced in the coexist system of EGCG and Zn2+. MMP-9 is thought to play a significant role in cancer cell migration and invasion. In the present paper, the results showed that EGCG suppressed the activity of MMP-9 in PC-3 cells in the presence of Zn2+, as a result, migration ability of the cells was significantly decreased.

The epidemiological studies and recent data have provided convinced evidence that green tea and its major constituent epigallocatechin gallate (EGCG) might have the potential to lower the risk of cancers in humans. Metal ions, such as zinc and cadmium, which are necessary to our health, are important factors inducing many diseases including prostate cancer in the condition of absence or excess. EGCG can satisfactorily exhibit complex chemistry with metal ions because of multiple hydroxyl states, which in turn changes their bioactivities and metabolism pathways. This paper presents the results of an investigation of the cytotoxicity of EGCG against PC-3 prostate cancer cells in the presence and absence of Cd2+ in vitro. The results showed that both EGCG and Cd2+ suppressed viability and clonegenecity of PC-3 cells, and the suppression effect was enhanced when EGCG added with Cd2+. Although Cd2+ up-regulated the 67 kDa laminin receptor (67LR), which is a migration-associated protein, the cell migration ability was not significantly increased after each treatment. We also found that EGCG and Cd2+ directly interacted with mitochondrial, and the mixture of EGCG and Cd2+ (EGCG+Cd2+) significantly caused loss of the mitochondrial membrane potential, decrease of the ATP content and activation of caspase-9 compared with EGCG treated alone. Taken together, these findings suggest that Cd2+ enhanced the cytotoxicity of EGCG to PC-3 cells by up-regulating the 67LR and the mitochondria-mediated apoptosis pathway.

Epigallocatechin-3-gallate (EGCG), a major component of green tea, has both preventive and therapeutic beneficial actions in prostate cancer. In the present study, we compared the growth inhibitory effects and the antioxidant and ability to modify cell membrane permeation of zinc-EGCG complex and Zn2+/EGCG mixture on androgen-insensitive prostate cancer (PC-3) cells. It was noted that free Zn2+ enhanced the growth inhibitory effects of EGCG on PC-3 cells at 160 micromol/L concentration,whereas zinc-EGCG complex was ineffective. EGCG showed potent free radical scavenging ability in the presence of Zn2+. EGCG in the presence of Zn2+ was more effective than EGCG alone in enhancing the permeability of the cell membrane, whereas zinc-EGCG complex had no effect on PC-3 cell membrane permeability. These results indicate that though Zn2+ enhanced the action of EGCG on PC-3 cells, zinc-EGCG complex is highly unlikely to be formed in the presence of Zn2+ and EGCG to explain the potentiating action of Zn2+ on the growth inhibitory property of EGCG on PC-3 cells.