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Experimental and Molecular Therapeutics 33: Cellular and Molecular Pharmacology

The role of bile acids in cellular invasiveness of gastric cancer

Yu-Chung Wu, Chia-Li Lu, Kuan-Hua Chen, Chang-Fang Chiu and Chung-Tsen Hsueh
Yu-Chung Wu
Veterans General Hospital and National Yang Ming University, Taipei, Taiwan Republic of China, China Medical University Hospital, Taichung, Taiwan Republic of China, University of Kansas Medical Ctr., Kansas City, KS
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Chia-Li Lu
Veterans General Hospital and National Yang Ming University, Taipei, Taiwan Republic of China, China Medical University Hospital, Taichung, Taiwan Republic of China, University of Kansas Medical Ctr., Kansas City, KS
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Kuan-Hua Chen
Veterans General Hospital and National Yang Ming University, Taipei, Taiwan Republic of China, China Medical University Hospital, Taichung, Taiwan Republic of China, University of Kansas Medical Ctr., Kansas City, KS
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Chang-Fang Chiu
Veterans General Hospital and National Yang Ming University, Taipei, Taiwan Republic of China, China Medical University Hospital, Taichung, Taiwan Republic of China, University of Kansas Medical Ctr., Kansas City, KS
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Chung-Tsen Hsueh
Veterans General Hospital and National Yang Ming University, Taipei, Taiwan Republic of China, China Medical University Hospital, Taichung, Taiwan Republic of China, University of Kansas Medical Ctr., Kansas City, KS
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DOI:  Published May 2005
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Proc Amer Assoc Cancer Res, Volume 46, 2005

Abstract

4100

Bile acids have been implicated in the development of digestive tract malignancy such as colonic, gastric and esophageal neoplasms by epidemiological, clinical and animal studies. Several studies have shown that the growth and transformation signaling by most of the bile acids is through the activation of protein kinase C (PKC) and induction of cyclooxygenase-2 (COX-2) gene expression. The highly hydrophobic bile acids such as chenodeoxycholic acid (CD) and deoxycholic acid can promote carcinogenesis and stimulate the invasion of colon cancer cells. On the contrary, ursodeoxycholic acid (UDCA), a less hydrophobic stereoisomer of CD, inhibits proliferation and induces apoptosis in colon cancer cells. We have examined the effects of bile acid on human gastric cancer cells MKN-74. Exposure of CD led to activation of PKC alpha, increased COX-2 gene expression and increased prostaglandin E2 (PGE2) synthesis. The induced COX-2 protein expression could be detected within 4-h exposure of 200 μM CD, and it was dose- and time-dependent. PGE2 is the product of COX-2, and has been reported to cause tumor invasion and angiogenesis in animal study. Safingol, a PKC inhibitor, and thalidomide could suppress CD-induced COX-2 protein expression and PGE2 production. UDCA suppressed CD-induced PGE2 production but not COX-2 protein expression. Using a Boyden chamber invasion assay, both safingol and UDCA could impede CD-induced tumor invasiveness by 30-50%. Our results indicate that signaling of hydrophobic bile acid such as CD in gastric cancer is probably through PKC activation and COX-2 induction, which may give rise to anti-apoptosis, invasion and angiogenesis. By perturbing the bile acid pool, UDCA can attenuate CD-induced PGE2 synthesis and tumor invasiveness. UDCA holds a great potential as anti-cancer and chemopreventive agent in gastric cancer. (Supported by China Medical University Hospital DMR-91-032 and Taiwan National Science Council 91-2314-B-039-006.)

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Cancer Research: 65 (9 Supplement)
May 2005
Volume 65, Issue 9 Supplement
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The role of bile acids in cellular invasiveness of gastric cancer
Yu-Chung Wu, Chia-Li Lu, Kuan-Hua Chen, Chang-Fang Chiu and Chung-Tsen Hsueh
Cancer Res May 1 2005 (65) (9 Supplement) 967;

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The role of bile acids in cellular invasiveness of gastric cancer
Yu-Chung Wu, Chia-Li Lu, Kuan-Hua Chen, Chang-Fang Chiu and Chung-Tsen Hsueh
Cancer Res May 1 2005 (65) (9 Supplement) 967;
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