Abstract
We observed that free bile acids (CA, DCA, and CDCA) inhibited the growth of cholangiocarcinoma cells by promoting cell apoptosis, while the conjugated bile acids (GCA, GDCA, and GCDCA) stimulated cell growth. Consistently, we found that GDCA stimulated tumor growth and CDCA decreased tumor growth in xenografted mice. Further, the phosphorylated IkB was downregulated by free bile acids, and was upregulated by the conjugated bile acids. IL-6 and COX-2 were decreased by the free bile acids and increased by the conjugated bile acids. Collectively, these results suggest that the bile acids regulate the growth of cholangiocarcinoma by modulating NF-kB pathway.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Bile Acids and Salts / pharmacology*
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Cell Growth Processes / drug effects
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Cell Line, Tumor
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Cell Survival / drug effects
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Cholangiocarcinoma / drug therapy*
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Cholangiocarcinoma / metabolism
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Cholangiocarcinoma / pathology*
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Cyclooxygenase 2 / biosynthesis
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Cyclooxygenase 2 / genetics
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Disease Models, Animal
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Humans
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I-kappa B Proteins / metabolism
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Immunohistochemistry
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Interleukin-6 / biosynthesis
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Interleukin-6 / genetics
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Mice
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Mice, Nude
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NF-kappa B / metabolism*
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Phosphorylation / drug effects
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RNA, Messenger / biosynthesis
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RNA, Messenger / genetics
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Random Allocation
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Real-Time Polymerase Chain Reaction
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Xenograft Model Antitumor Assays
Substances
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Bile Acids and Salts
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I-kappa B Proteins
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Interleukin-6
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NF-kappa B
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RNA, Messenger
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Cyclooxygenase 2