To investigate the roles and mechanism(s) of epigallocatechin gallate (EGCG) in carcinogenesis in malignant transformed cell line, cadmium-induced malignant transformed cells were treated with different doses of EGCG. Then cell proliferation, cell apoptosis, hTERT mRNA and protein level, and c-Myc protein levels were measured at different time points. EGCG was found to inhibit cell proliferation in a dose-dependent manner. Cell cycle was changed in the transformed cells after EGCG treatment with significantly increased cell numbers in G0/G1 phase and decreased cell numbers in S phase compared to control group, P < 0.001. EGCG was also found to promote cell apoptosis with a time-dependent manner. Both mRNA and protein levels of hTERT gene were significantly decreased in cells after treated with EGCG, P < 0.001. c-Myc protein level was significantly decreased after EGCG treatment, especially in the highest dose group (i.e. 200 μg/ml). The decrease in c-Myc protein level was accompanied by the reduction of hTERT protein levels. EGCG can inhibit cell proliferation and promote apoptosis in malignant cadmium-transformed cell line. The mechanism may be its ability to reduce c-Myc gene expression and consequently inhibits hTERT gene expression, which in turn decrease the telomerase activity.
Keywords: Tea polyphenols; apoptosis; cadmium; cell proliferation; telomerase.