实用肿瘤学杂志 ›› 2010, Vol. 24 ›› Issue (3): 220-223.doi: 10.3969/j.issn.1002-3070.2010.03.006

• 论著 • 上一篇    下一篇

全反式维甲酸对MAPK信号传导通路的影响

杨悦1, 杨艳梅1, 孙根2, 张春艳1, 秦莉1, 袁玉涛1, 马玉彦1   

  1. 1.哈尔滨医科大学肿瘤研究所(哈尔滨 150081);
    2.肇东市人民医院普外科
  • 收稿日期:2010-05-17 出版日期:2010-06-28 发布日期:2015-01-24
  • 通讯作者: 杨艳梅,E-mail:yangym0916@163.com
  • 作者简介:杨悦,男,(1979-),本科,助理研究员,从事恶性肿瘤的预防及治疗的基础研究
  • 基金资助:
    黑龙江省教育厅资助课题(11521182)

Effects of all trans-retinoic acid on the expression of MAPK signal transduction pathway in gastric carcinoma cell line

YANG Yue1, YANG Yanmei1, SUN Gen2, ZHANG Chunyan1, QIN Li1, YUAN Yutao1, MA Yuyan1   

  1. 1.Harbin Medical University Cancer Research Institute,Harbin 150081;
    2.The People′s Hospital of Zhao dong City
  • Received:2010-05-17 Online:2010-06-28 Published:2015-01-24

摘要: 目的 研究全反式维甲酸(all trans retinoic acid,ATRA)对人胃腺癌细胞株(SGC-7901)丝裂原激活的蛋白激酶(Mitogen activated protein kinase,MAPK)信号转导通路的影响。方法 采用四甲基偶氮唑盐(MTT)方法检测ATRA对SGC-7901细胞增殖的抑制作用;Western blot方法检测不同浓度ATRA处理后的SGC-7901细胞ERK1/2、P38、JNK及其磷酸化蛋白的表达情况。结果 10-9mol/L-10-5mol/L的ATRA作用SGC-7901细胞48h,能显著抑制细胞增殖,其抑制率分别为(10.2±0.5)%、(15.3±0.5)%、(17.0±0.7)%、(28.4±1.0)%和(36.9±0.7)%;Western blot检测显示ATRA对细胞中ERK1/2、P38、JNK及p-JNK蛋白的表达没有明显影响,但p-ERK1/2蛋白显著减少,p-P38蛋白明显增加。结论 ATRA抑制SGC-7901细胞增殖可能与其调节ERK1/2 MAPK和P38 MAPK途径有关。

Abstract: Objective To investigate the effects of all trans-retinoic acid(ATRA)on the expression of MAPK signal transduction.Methods The effects of ATRA on the cell proliferation was measured by methyl thiazolyl tetrazolium(MTT),and the expression of ERK1/2,P38,JNK and their phosphorylated proteins were measured by Western blot.Results The inhibitory rate was 10.2%±0.5%,15.3%±0.5%,17.0%±0.7%,28.4%±1.0% and 36.9%±0.7%,respectively,as SGC-7901 cells were exposed to 10-9mol/L-10-5mol/L ATRA for 48 hours.ATRA did not influence the expression of ERK1/2,P38,JNK and p-JNK,but significantly decreased p-ERK1/2,significantly increased p-P38.Conclustion It is suggested that ATRA could inhibit proliferation of SGC-7901 cells via regulating the ERK1/2 and P38 MAPK pathway.

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