Carcinogenesis Advance Access originally published online on December 4, 2003
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Carcinogenesis, Vol. 25, No. 3, 419-423,
March 2004
Carcinogenesis vol.25 no.3 © Oxford University Press 2004; all rights reserved.
CARCINOGENESIS |
Bile acids induce cyclooxygenase-2 expression in human pancreatic cancer cell lines
1 Departments of Surgery and 2 Medicine, New York Presbyterian Hospital and Weill Medical College of Cornell University, New York, NY 10021, USA and 3 Strang Cancer Prevention Center, New York, NY 10021, USA
To investigate a possible link between bile acids and the pathogenesis of pancreatic cancer, we determined whether conjugated or unconjugated bile acids induced cyclooxygenase-2 (COX-2) in two human pancreatic cancer cell lines, BxPC-3 and SU 86.86. Bile acids are known promoters of gastric and colon cancer. We demonstrated previously that COX-2, an enzyme that catalyzes the synthesis of prostaglandins, is over-expressed in human pancreatic adenocarcinoma. Both human pancreatic cell lines were treated with conjugated and unconjugated bile acids. COX-2 mRNA and protein were determined. In addition, prostaglandin E2 (PGE2) synthesis was measured. Treatment with conjugated or unconjugated bile acids for 3 h up-regulated COX-2 mRNA. Chenodeoxycholate (CD) or deoxycholate at concentrations ranging from 12.5 to 100 µM caused a dose-dependent induction of COX-2 protein with a maximal effect at 100 µM. Induction of COX-2 protein by CD and deoxycholate was detected after treatment for 6 h with maximal induction at 12 h. Taurochenodeoxycholate, a conjugated bile acid, also caused dose-dependent induction of COX-2 but higher concentrations of bile acid (200–1200 µM) were required. Levels of cyclooxygenase-1 were unaffected by bile acid treatment. Unconjugated and conjugated bile acids caused 7- and 4-fold increases in PGE2 production, respectively. Taken together, these findings suggest a possible role for bile acids in the pathogenesis of pancreatic cancer.
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