Objectives: This study investigates the mechanism of SCE-induced apoptosis in AGS human gastric cancer cells. Materials and methods: SCE concentrations from 100 to 400 mg/ml were used. Cell viabilities were determined using MTT assay. Members of the Bcl-2 family and Bax were detected by Western blotting. RT-PCR was performed to measure the expression level of the Fas/FasL pro-apoptotic genes.Results: SCE inhibited the proliferation AGS cells for 24 or 72 h (inhibition by 3.1% ± 5.2% at 100 mg/ml and 87.3% ± 7.6% at 400 mg/ml at 24 h and by 40.2% ± 5.3% 100 mg/ml and 95.3% ± 1.3% 400 mg/ml at 72 h) and increased the sub-G1 phase (25.3% ± 5.2% at 100 mg/ml and 370.2% ± 7.2% at 400 mg/ml) and the mitochondrial membrane depolarization (11.2% ± 2.1% at 100 mg/ml and 311.5% ± 6.1% at 400 mg/ml). The SCE-induced apoptotic cell death showed the down-regulation of Bcl-2, but up-regulation of Bax. Subsequently, SCE increased the expression level of Fas/FasL, activated caspase-9 and -3, and increased reactive oxygen species generation. Also, JNK II inhibitor or a p38 MAPK inhibitor inhibited SCE-induced cell death. Discussion and conclusion: These results indicate that SCE might be an effective chemotherapeutic for the treatment of human gastric cancer.