在東南亞國家胃癌是常見的原發性惡性腫瘤。在發展胃癌治療策略時，應用藥物進入臨床試驗階段前，實驗動物模式是非常重要。MGCC3I 和MGCC3I-B2 細胞是小鼠胃癌細胞株，最初來自 ICR 小鼠原位胃癌動物模式。在過去的研究，丙酮酸乙酯（EP）具有抗發炎的特性和抗胃癌生長效果。本研究的目的是探討在體外培養胃癌細胞株給予丙酮酸乙酯（ethyl pyruvate, EP）處理對細胞生長和細胞週期的作用。其次，在原位胃癌動物模式評估丙酮酸乙酯的免疫治療效用。丙酮酸乙酯藥物敏感性試驗的評估，是將癌細胞培養在6公分培養盤並用不同濃度（0.5，1，2.5和5 mM）的丙酮酸乙酯處理，在不同時間點收集細胞，使用台盼藍溶液染色及血球計數器計數活細胞數目。癌細胞的細胞週期分析是採用碘化丙啶分析法。探討丙酮酸乙酯免疫抗癌作用是將小鼠胃癌細胞株MGCC3I-B2 種植於ICR小鼠胃部，癌細胞種植後第六天，在動物飲水中加入1％丙酮酸乙酯，癌細胞生長至第十四天犧牲小鼠，取出胃部腫瘤，去除胃內容物並稱重。結果顯示丙酮酸乙酯減少MGCC3I 和MGCC3I-B2細胞株的細胞生長，此作用具有時間和濃度依賴性。在MGCC3I-B2胃癌細胞株，丙酮酸乙酯會誘發細胞的細胞週期阻滯在G2/M期。丙酮酸乙酯顯著抑制小鼠胃部腫瘤生長。綜合以上，我們建議丙酮酸乙酯具有胃癌治療的潛力，可提供抗癌效用。 Gastric cancer is one of the most common primary malignancies of the stomach in East Asian countries. Experimental animal models were required to develop therapeutic strategies for the treatment of gastric cancer before potential therapeutic targets can enter clinical trials. The MGCC3I and MGCC3I-B2 cells, mouse gastric cancer cell lines, were originally derived from orthotopic transplantable gastric cancer in ICR mice. In previous studies, ethyl pyruvate（EP） has anti-inflammatory properties and anti-tumor effects on the growth of gastric cancer.The aim of this study is to investigate the effect of EP on the cell growth and cell cycle of gastric cancer in vitro. Moreover, the immunological therapeutic effect of the EP was evaluated in this animal tumor model in vivo. To assess the chemosensitivity to EP, tumor cells were plated onto 6 cm plate and incubated with various concentrations（0.5, 1, 2.5 and 5 mM）of EP. Tumor cells were harvested at various time intervals to determine the number of viable cells on a hemocytometer and used the Trypan blue exclusion method. Tumor cells were analyzed for cycle changes by propidium iodide analysis. To investigate the immunological antitumor effects of EP, MGCC3I-B2 cells were implanted orthotopically into the stomachs of ICR mice. EP was administered via a 1％ solution available ad libitum in animal drinking water beginning on Day 6 postimplantation. The mice were sacrificed 14d after tumor cell implantation. The whole stomachs from mice were excised, washed, removed of remaining diet, and weighed.The results demonstrated that EP diminished the cell growth of MGCC3I and MGCC3I-B2 cells in a time-and concentration-dependent manner. EP induced cell cycle arrests at the G2/M phase in MGCC3I-B2 cells. Tumor growth was significantly inhibited by EP in vivo. Taken together, we suggest that EP may have therapeutic potential in gastric cancer therapy, in part, which possibly contributed to the potent antitumor effect.