Journal
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
Volume 306, Issue 4, Pages 887-897Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/S0006-291X(03)01079-9
Keywords
prostaglandin; COX-2; pancreatic cancer; VEGF; EP receptor; autocrine loop
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In some cancers cyclooxygenase (COX) inhibition appears to be anti-mitogenic and anti-angiogenic, but the actions of COX-derived prostaglandins in pancreatic cancer (PaCa) are unknown. In this study COX-2 was detected in three of six PaCa cell lines while COX-1 was identified in all cell lines. COX-2 expression correlated with basal and arachidonic acid (AA) stimulated PGE(2) production. PGE(2) production was inhibited by the COX-2 inhibitor nimesulide. In COX-2 expressing cells, exogenous AA and PGE(2) increased VEGF synthesis via the EP2 receptor. Whereas PGE, stimulated intracellular cAMP formation in COX-2 positive and negative cells, 8-bromo cAMP stimulated VEGF production only in COX-2 expressing cells. Stimulating COX-2 expressing PaCa cell lines with AA enhanced migration of endothelial cells, an effect which was inhibited by a COX-2 inhibitor and EP2 receptor antagonist. These data identify a subset of human PaCa cell lines that express functional COX-2 enzyme. PGE, generated by specific COX-2 activity increases VEGF secretion in human PaCa cells through an autocrine mechanism. (C) 2003 Elsevier Science (USA). All rights reserved.
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