Ethyl pyruvate inhibits cell growth of murine gastric cancer cells by inducing cell cycle arrest

碩士 === 嘉南藥理科技大學 === 生物科技系 === 101 === 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 cl...

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Bibliographic Details
Main Authors: Hui-Chun Tsai, 蔡蕙君
Other Authors: Yi-Pey Luo
Format: Others
Language:zh-TW
Published: 2013
Online Access:http://ndltd.ncl.edu.tw/handle/78839561237743108906
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Summary:碩士 === 嘉南藥理科技大學 === 生物科技系 === 101 === 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.