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Carcinogenesis Advance Access published online on December 20, 2006
Carcinogenesis, doi:10.1093/carcin/bgl249
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Published by Oxford University Press 2006.

Spontaneous hepatocarcinogenesis in farnesoid X receptor-null mice

Insook Kim, Keiichirou Morimura, Yatrik Shah, Qian Yang, Jerrold M. Ward and Frank J. Gonzalez

Laboratory of Metabolism, National Cancer Institute, National Institutes of Health, Bethesda Maryland, 20892

Correspondence: Frank J. Gonzalez. Building 37, Room 3106, Laboratory of Metabolism, National Cancer Institute, National Institutes of Health, Bethesda Maryland, 20892. Email: fjgonz{at}helix.nih.gov; Phone: 301-496-9067; Fax: 301-496-8409

The farnesoid X receptor (FXR) controls the synthesis and transport of bile acids. Mice lacking expression of FXR, designated Fxr-null, have elevated levels of serum and hepatic bile acids and an increase in bile acid pool size. Surprisingly, at 12 months of age, male and female Fxr-null mice had a high incidence of degenerative hepatic lesions, altered cell foci and liver tumors including hepatocellular adenoma, carcinoma and hepatocholangiocellular carcinoma, the latter of which are rarely observed in mice. At 3-months, Fxr-null mice had increased expression of the proinflammatory cytokine IL-1ß mRNA and elevated ß-catenin and its target gene c-myc. They also had increased cell proliferation as revealed by increased PCNA mRNA and BrdU incorporation. These studies reveal a potential role for FXR and bile acids in hepatocarcinogenesis.

Key Words: farnesoid X receptor • c-Myc • Il-1ß • ß-catenin • PCNA • bromodeoxyuridine


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