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Helicobacter pylori modulates cyclooxygenase-2 and 15-hydroxy prostaglandin dehydrogenase in gastric cancer.
Oncology Letters 2017 November
Persistent infection with Helicobacter pylori may contribute to the carcinogenesis of gastric cancer through modulating local prostaglandin E2 (PGE2) levels. Cyclooxygenase-2 (COX-2) and 15-hydroxy prostaglandin dehydrogenase (15-PGDH) are two key enzymes that regulate PGE2 synthesis and inactivation, respectively. The present study was designed to investigate the expression of COX-2 and 15-PGDH in gastric cancer specimens (n=66) in comparison to that of control specimens (n=70) and, furthermore, to semi-quantitatively assess the level of COX-2 and 15-PGDH mRNA and protein in tissues with or without H. pylori infection by reverse transcription-polymerase chain reaction and immunohistochemistry, respectively. It was revealed that COX-2 was expressed in almost all gastric cancer specimens infected with H. pylori (32 out of 33 specimens), but it was also expressed in 2/3 gastric cancers without H. pylori infection (22 out of 33 specimens). By contrast, COX-2 was expressed in <1/6 control subjects regardless of H. pylori infection. Furthermore, 15-PGDH was expressed in control samples but significantly downregulated in gastric cancer specimens. H. pylori infection resulted in slight inhibition of 15-PGDH in control subjects, but significant inhibition of 15-PGDH mRNA expression and protein synthesis in the gastric cancer specimens. These findings indicated that COX-2 and 15-PGDH, the two enzymes that regulate PGE2 levels, were significantly altered in gastric cancer, and that H. pylori may contribute to gastric carcinogenesis through modulating COX-2 and 15-PGDH mRNA expression and protein synthesis.
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