Background: Curcumin is a valuable abstract from anticancer plant, which can inhibit cell growth and induce apoptosis of several carcinomas. Aims: To appraise the inhibitory effects of curcumin on proliferation of gastric carcinoma cells and its possible mechanism. Methods: ①Human gastric adenocarcinoma cell line SGC7901 was cultured routinely and treated by curcumin in different concentrations. The cell growth was detected with methyl thiazolyl tetrazolium (MTT) method. ②The gastric adenocarcinoma cell line SGC7901 was treated with curcumin in different concentrations. Then, the epidermal growth factor receptor (EGFR) expression of the cells was detected by immuno;fluorescent staining and flow cytometry (FCM). ③The gastric adenocarcinoma cell line SGC7901 was treated with curcumin in low concentration or with transforming growth factor alpha (TGF;α), or with the two substances simultaneously in low concentrations. The cell growth rate was detected by MTT method and the inhibition rate was calculated. Results: ①Cell proliferation was inhibited markedly by curcumin in a dose;dependent manner. When the cells were treated by 10 μmol/L, 20 μmol/L and 30 μmol/L curcumin for 72 hours, the inhibition rates of cell proliferation were 22.4%, 46.9% and 67.2%, respectively. ②The EGFR expression of the cells declined significantly when treated with curcumin. Given 10 μmol/L, 20 μmol/L and 30 μmol/L curcumin for 48 hours, the EGFR expression decreased by 10.5%, 17.1% and 30.0%, respectively. ③No change occurred when the cells were treated with low concentration of curcumin at 5 μmol/L for 72 hours. When the cells were treated with TGF;α 30 μg/L, the cell proliferation rate accelerated markedly, but when the cells were treated with curcumin 5 μmol/L and TGF;α 30 μg/L, the cell proliferation stimulated by TGF;α was markedly inhibited by curcumin with an inhibition rate of 21.5%. Conclusions: Curcumin can inhibit the proliferation of gastric adenocarcinoma cells, and inhibit the EGFR expression. Furthermore, it can inhibit the cell proliferation stimulated by TGF;α.