EGCG induced apoptosis and expression change of bcl-2 protein in gastric and hepatic carcinoma cells

Objective: To investigate whether (-) - epigallocatechi n- 3 -gallate (ECCG) could induce apoptosi s and affect apoptosis - associated gene bc1-2 expression in gastric carcinoma MGC-803 cells and hepatic carcinoma BEL-7402 cells. Methods: Growth suppression, apoptosis-related alterations in morphology and biochemistry, and change in expression of bc1-2 were determined after EGCG treatment for MGC-803 and BEL-7402 cell lines by using tetrazolium salt MTh assay, gel electrophoresis and flow cytometry. Results: EGCG inhibited the growth of MGC-803 cells and BEL-7402 cells in a dose-dependent manner, with IC50 values of 188. 52 and 264. 53 pg/ml, respectively. Treatment of MGC-803 cells and BEL-7402 cells with 200 ~ 300 μg/ml EGCG for 24 ~ 36 h resulted in apoptosis-associated alterations: ladderbands on agarose gel electrophoresis and hypodiploid peaks on flow cytometric histogram. Moreover, EGCG downregulated bc1-2 expression in MGC-803 cells and BEL-7402 cells with time-dependence. Conclusion: EGCG has the inhibitory effects on the growth of gastric carcinoma MGC-803 cells andhepatic carcinoma BEL-7402 cells, and one of the mechanisms could be the induction of apoptosis in the two tumor cell lines.The apoptosis is associated with GCG-induced decrease of the bc1-2 protein level in MGC-803 and BEL-7402 cell lines.