Helicobacter pylori promote gastric cancer cells invasion through a NF-κB and COX-2-mediated pathway

Chun Ying Wu, Chau Jong Wang, Chi Chuan Tseng, Hsiao Ping Chen, Ming Shing Wu, Jaw Town Lin, Hiroyasu Inoue, Gran Hum Chen*

*此作品的通信作者

研究成果: Article同行評審

90 引文 斯高帕斯(Scopus)

摘要

Aim: To examine the effects of Hekicobacter pylori (H pylori) infection on the invasiveness of gastric cancer cells, and to elucidate its mechanism. Methods: Gastric carcinoma cells, MKN-45, were incubated with CagA-positive H pylori, and cell invasion was determined by Matrigel analysis. The expression of matrix metalloproteinase-9 (MMP-9), vascular endothelial growth factor (VEGF), and cyclooxygenase-2 (COX-2) were assessed by Western-blot analysis, and transcriptional activation of the COX-2 promoter was examined by measuring luciferase and β-galactosidase activities. Lastly, the protein-DNA interaction was confirmed by an electrophoretic mobility shift assay. Results: The current studies showed that: (1) incubation of CagA-positive H pylori with MKN-45 cells significantly promotes gastric cancer cells invasion, and this effect is attenuated by pre-treatment with NS-398, a COX-2 inhibitor, or PDTC, a nuclear factor κB (NF-κB) inhibitor; (2) the induction of MKN-45 cells invasion by H pylori is associated with increases in COX-2, MMP-9, and VEGF protein expression, and co-incubation of NS-398 or PDTC significantly reduces these effects; (3) H pylori infection transactivates COX-2 promoter activity and increases the binding of NF-κB to this promoter. Conclusion: Our data demonstrate that H pylori infection promotes gastric epithelial cells invasion by activating MMP-9 and VEGF expression. These effects appear to be mediated through a NF-κB and COX-2 mediated pathway, as COX-2 or NF-κB inhibitor significantly attenuate the invasiveness of gastric cancer cells and the expressions of MMP-9 and VEGF protein.

原文English
頁(從 - 到)3197-3203
頁數7
期刊World Journal of Gastroenterology
11
發行號21
DOIs
出版狀態Published - 7 6月 2005

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