To investigate the molecular mechanism involved in the downregulation of vascular endothelial growth factor(VEGF) expression through the suppression of signal transducer and activator of transcription 3(Stat3) by(-)-Epigallocatechin-3-gallate (EGCG).After human gastric cancer cells (AGS) were treated with IL-6 (50 μg/L) and EGCG(0, 5, 10, 25 or 50 μmol/L), the expression levels of VEGF, total Stat3(tStat3), and activated Stat3(pStat3) in tumor cells were examined by Western blotting. The influence of the inhibitor of Stat3 pathway on the IL-6-induced VEGF expression was investigated. VEGF protein level in tumor cell culture medium was determined by ELISA and VEGF mRNA expression in tumor cells by RT-PCR. Tumor cell nuclear extract was prepared and nuclear expression of pStat3 was detected. Stat3-DNA binding activity was examined with chromatin immunoprecipitation (ChIP) assay.IL-6 significantly increased VEGF expression in AGS gastric cancer cells. Compared with the group without IL-6, the expression and secretion of VEGF protein, and mRNA expression increased by 2.4 fold,2.8 fold, and 3.1 fold(all P0.05). Stat3 nuclear translocation and Stat3-DNA binding activity in AGS cells or that induced by IL-6 were directly inhibited by EGCG(P<0.05).EGCG reduces expression of VEGF in gastric cancer cells through the inhibition of Stat3 activity.