Despite recognition of the devastating malignant potential of the pancreatic ductal cancer, the exact pathophysiological events contributing to tumor growth remain to be elucidated. Expression levels of inducible nitric oxide synthase (iNOS) and cyclooxygenase (COX)-2 were found to be frequently elevated in several types of human cancer and have also been directly linked to carcinogenesis. The purpose of this study was to determine the expression of COX-1, COX-2 and iNOS in human pancreatic cancer and matched normal adjacent tissue by the Western blot assay. Marked COX-2 expression was observed in cancer tissue compared with the normal surrounding tissue. The iNOS protein was markedly expressed only in pancreatic cancer while the expression of COX-1 was similar in both normal and cancerous tissue. Our findings indicate that COX-2 up-regulation and the expression of iNOS in pancreatic cancer, not seen in normal tissue, may play a role in the pathogenesis of human pancreatic adenocarcinomas. These observations suggest that COX-2 and iNOS may be a target for prevention or treatment of pancreatic carcinomas.
Increased expression of inducible nitric oxide synthase and cyclooxygenase-2 in pancreatic cancer
FRANCO, Luigina;DORIA, Denise;BERTAZZONI MINELLI, Elisa;BENINI, Anna;BASSI, Claudio
2004-01-01
Abstract
Despite recognition of the devastating malignant potential of the pancreatic ductal cancer, the exact pathophysiological events contributing to tumor growth remain to be elucidated. Expression levels of inducible nitric oxide synthase (iNOS) and cyclooxygenase (COX)-2 were found to be frequently elevated in several types of human cancer and have also been directly linked to carcinogenesis. The purpose of this study was to determine the expression of COX-1, COX-2 and iNOS in human pancreatic cancer and matched normal adjacent tissue by the Western blot assay. Marked COX-2 expression was observed in cancer tissue compared with the normal surrounding tissue. The iNOS protein was markedly expressed only in pancreatic cancer while the expression of COX-1 was similar in both normal and cancerous tissue. Our findings indicate that COX-2 up-regulation and the expression of iNOS in pancreatic cancer, not seen in normal tissue, may play a role in the pathogenesis of human pancreatic adenocarcinomas. These observations suggest that COX-2 and iNOS may be a target for prevention or treatment of pancreatic carcinomas.
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