Suppr超能文献

幽门螺杆菌通过p38丝裂原活化蛋白激酶/活化转录因子2信号通路增强MKN45细胞中环氧合酶2的表达。

Helicobacter pylori enhances cyclooxygenase 2 expression via p38MAPK/ATF-2 signaling pathway in MKN45 cells.

作者信息

Li Qi, Liu Ningning, Shen Bo, Zhou Lihong, Wang Yan, Wang Yiqin, Sun Jue, Fan Zhongze, Liu Rui Hai

机构信息

Department of Oncology, Putuo Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai 200062, China.

出版信息

Cancer Lett. 2009 Jun 8;278(1):97-103. doi: 10.1016/j.canlet.2008.12.032. Epub 2009 Feb 6.

Abstract

The over-expression of COX-2 (Cyclooxygenase 2) protein has been reported to play a key role in the incidence and development of Helicobacter pylori-associated gastric cancer. The induction of COX-2 in the gastric cancer cells with H. pylori has been demonstrated previously, but little is known about the mechanism. This study reported that the COX-2 mRNA and proteins expression level and the activity of COX-2 promoter increased remarkably with H. pylori stimulation in the MKN45 gastric cancer cells. H. pylori also stimulated phosphorylation of p38MAPK and ATF-2, which is the downstream kinase of p38MAPK. Moreover, the expression levels of COX-2 were suppressed with p38MAPK inhibitor treatment. These results suggest that H. pylori-induced activation of p38MAPK/ATF-2-mediated signal pathway is necessary for the expression of COX-2.

摘要

据报道,COX-2(环氧化酶2)蛋白的过度表达在幽门螺杆菌相关胃癌的发生和发展中起关键作用。先前已证明幽门螺杆菌可诱导胃癌细胞中COX-2的产生,但对其机制了解甚少。本研究报道,在MKN45胃癌细胞中,幽门螺杆菌刺激后COX-2 mRNA和蛋白表达水平以及COX-2启动子活性显著增加。幽门螺杆菌还刺激p38MAPK和ATF-2(p38MAPK的下游激酶)的磷酸化。此外,用p38MAPK抑制剂处理可抑制COX-2的表达水平。这些结果表明,幽门螺杆菌诱导的p38MAPK/ATF-2介导的信号通路激活是COX-2表达所必需的。

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验