期刊
MOLECULAR MEDICINE REPORTS
卷 10, 期 4, 页码 2123-2129出版社
SPANDIDOS PUBL LTD
DOI: 10.3892/mmr.2014.2458
关键词
Helicobacter pylori; VEGF; p38 MAPK; COX-2; PGE(2); gastric cancer
资金
- National Natural Science Foundation of China [81072955, 81273958, 81202663]
- Program of Shanghai Municipal Education Commission [12ZZ118]
- Science and Technology Commission of Shanghai Municipality [12ZR1449300, 1214090250]
- Shanghai Municipal Health Bureau [2010019, XBR2011061, 2010044]
- Major Program of Technology Innovation, Putuo District, Shanghai [2009PTKW001]
Helicobacter pylori has been suggested to be the major cause of gastric malignancy. However, the pathogenesis and molecular mechanisms of gastric tumorigenesis induced by H. pylori infection are yet to be elucidated. In the present study, the expression levels of vascular endothelial growth factor (VEGF), which has been suggested to promote angiogenesis in gastric cancer, were found to be elevated in H. pylori-infected MKN45 cells. Furthermore, it was demonstrated that the expression of VEGF was modulated by the p38 mitogen-activated protein kinases (MAPK) pathway via regulation of the cyclooxygenase (COX)-2 pathway. It was also found that prostaglandin E2 (PGE(2)) and its receptor EP2/EP4 may mediate the upregulation of VEGF in gastric cells exposed to H. pylori. In combination, these results suggest that VEGF expression is regulated by the p38 MAPK COX-2-PGE(2)-EP2/EP4 pathway in gastric cancer cells induced by H. pylori. This provides a theoretical basis for the investigation of the pathogenesis of H. pylori-induced gastric cancer.
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