Role of COX-2 in the development of gastric tumor by Helicobacter Pylori

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Expression of COX-2 in human gastric mucosa with or without Helicobacter Pylori (H.pylori) Infection was immunohistochemically investigated. H.pylori infection induced the accumulation of neutrophils but not COX-2 expression in normal gastric mucosa. In the next step. Gastric pylyps were studied. COX-2 was strongly expressed in mesenchymal cells under the surface of gastric hyperplastic polyps. However, COX-2 was only weekly expressed in gastric adenomas Microvessel density was significantly collated with the expression of COX-2. These results suggest that COX-2 is related to the growth of hyperplastic polyp but not adenoma in stomach.Since COX-2 was mainly expressed in mesenchymal cells, it is postulated that prostaglandins (PGs, product of COX-2) accelerate growth of tumors and further cancer formation. This step may be mediated by angiogenesis. Therefore, we investigated the effect of PGs on VEGF production. PGs dramatically increased VEGF production by U-937 cells, A model of human macrophages. Changes of gene expression was studied by cDNA microarray using these cells. Among 10,000 genes, several of them were increased or decreased after treatment with PGs. Meaning of each gene will be studiedThis results suggest that in human gastric hyperplastic polyp H.pylori induces COX-2 expression in mesenchymal cells and promotes angiogenesis, development of tumor, and cancer formation.