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

被引：39
|
作者：
Li, Qi [1 ]
Liu, Ningning [1 ]
Shen, Bo [2 ]
Zhou, Lihong [1 ]
Wang, Yan [1 ]
Wang, Yiqin [3 ]
Sun, Jue [1 ]
Fan, Zhongze [1 ]
Liu, Rui Hai [4 ]
机构：
[1] Shanghai Univ Tradit Chinese Med, Dept Oncol, Putuo Hosp, Shanghai 200062, Peoples R China
[2] Fudan Univ, Inst Radiat Med, Shanghai 200032, Peoples R China
[3] Shanghai Univ Tradit Chinese Med, Shanghai 200032, Peoples R China
[4] Cornell Univ, Dept Food Sci, Ithaca, NY 14853 USA
来源：
CANCER LETTERS | 2009年 / 278卷 / 01期
基金：
中国国家自然科学基金;
关键词：
Gastric cancer; Helicobacter pylori; Cyclooxygenase; 2; p38MAPK; Signal transduction; GASTRIC EPITHELIAL-CELLS; NF-KAPPA-B; MONGOLIAN GERBILS; GROWTH-FACTOR; CANCER CELLS; AGS CELLS; ANGIOGENESIS; CARCINOMA; APOPTOSIS; MUCOSA;
D O I：
10.1016/j.canlet.2008.12.032
中图分类号：
R73 [肿瘤学];
学科分类号：
100214 ;
摘要：
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. pylon 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. Crown Copyright (c) 2009 Published by Elsevier Ltd. All rights reserved.
引用
收藏
页码：97 / 103
页数：7
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