首页 | 官方网站   微博 | 高级检索  
     

Effect of apoptosis on gastric adenocarcinoma cell line SGC—7901 induced by cis—9,trans—11—conjugated linoleic acid
作者姓名:Liu JR  Chen BQ  Yang YM  Wang XL  Xue YB  Zheng YM  Liu RH
作者单位:[1]FoodScienceandToxicology,DepartmentofFoodScience,ComellUniversity,Ithaca,NY14853-7201,USA [2]PublicHealthColleng,HarbinMedicalUniversity,Harbin150001,HeilongjiangProvince,China
摘    要:

关 键 词:胃腺癌细胞系  SGC-7901  亚麻酸衍生物  cis-9  trans-11  诱发凋亡

Effect of apoptosis on gastric adenocarcinoma cell line SGC-7901 induced by cis-9, trans-11-conjugated linoleic acid
Liu JR,Chen BQ,Yang YM,Wang XL,Xue YB,Zheng YM,Liu RH.Effect of apoptosis on gastric adenocarcinoma cell line SGC-7901 induced by cis-9, trans-11-conjugated linoleic acid[J].World Journal of Gastroenterology,2002,8(6):999-1004.
Authors:Liu Jia-Ren  Chen Bing-Qing  Yang Yan-Mei  Wang Xuan-Ling  Xue Ying-Ben  Zheng Yu-Mei  Liu Rui-Hai
Affiliation:1. Public Health College, Harbin Medical University, Harbin 150001, Heilongjiang Province, China
2. Food Science and Toxicology, Department of Food Science, Cornell University, Ithaca, NY 14853-7201, USA
Abstract:AIM: To determine the effect of apoptosis on gastric cancer cells (SGC-7901) induced by cis-9, trans-11-conjugated linoleic acid (c9, t11-CLA) and its possible mechanism in the inhibition of cancer cells growth. METHODS: Using cell culture, flow cytometery and immunocytochemical techniques, we examined the cell growth, frequency of apoptosis and distribution of cell cycle, expression of ki67, bcl-2, Fas, and c-myc of SGC-7901 cells which were treated with various c9, t11-CLA concentrations (25,50,100 and 200 micromol x L(-1)) of c9, t11-CLA for 24 h and 48 h, with a negative control (0.1 % ethanol). RESULTS: The growth of SGC-7901 cells was inhibited by c9,t11-CLA. Eight days after treatment with various concentrations of c9,t11-CLA, as mentioned above, the inhibition rates were 5.9 %, 20.2 %,75.6 % and 82.4 %, respectively. The frequency of apoptosis on SGC-7901 cells induced by different concentrations of c9, t11-CLA (except for 25 micromol.L(-1), 24 h) was significantly greater than that in the negative control (P<0.01). To further investigate the influence of the cell cycle progression, we found that apoptosis induced by c9, t11-CLA may be involved in blocking the cell cycle of SGC-7901 cells. Immunocytochemical staining demonstrated that SGC-7901 cells preincubated in media supplemented with different c9, t11-CLA concentrations for various time periods significantly decreased the expressions of ki67 (the expression rates were 18.70-3.20 %, at 24 h and 8.10-0.20 % at 48 h, respectively), bcl-2 (4.30-0.15 % at 24 h and 8.05 %-0 at 48 h), and c-myc (4.85-2.20 % at 24 h and 4.75-0.30 % at 48 h) as compared with those in the controls (the expressions of ki67, bcl-2, and c-myc were 15.1 % at 24 h and 13.5 % at 48 h, 6.80 % at 24 h and 8.00 % at 48 h, 5.50 % at 24 h and 5.30 % at 48 h, respectively) (P<0.01), whereas the expressions of Fas were increased (0.60-2.75 %, 24 h and 0.45-5.95 %, 48 h). CONCLUSION: The growth and proliferation of SGC-7901 cells are inhibited by c9, t11-CLA via blocking the cell cycle, pathways of bcl-2-associated mitochondria with reduced expression of bcl-2 and Fas-associated death domain protein (FADD) with enhanced expression of Fas. But expression of c-myc on SGC-7901 cells is lower than that in negative control, which needs to be studied further.
Keywords:
本文献已被 维普 万方数据 PubMed 等数据库收录!
设为首页 | 免责声明 | 关于勤云 | 加入收藏

Copyright©北京勤云科技发展有限公司    京ICP备09084417号-23

京公网安备 11010802026262号