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Article: Dysregulated hepatic bile acids collaboratively promote liver carcinogenesis

TitleDysregulated hepatic bile acids collaboratively promote liver carcinogenesis
Authors
Keywordsbile acids
gut microbiota
inflammation
liver carcinogenesis
proliferation
Issue Date2016
Citation
International Journal of Cancer, 2016, v. 139, n. 8, p. 1764-1775 How to Cite?
AbstractDysregulated bile acids (BAs) are closely associated with liver diseases and attributed to altered gut microbiota. Here, we show that the intrahepatic retention of hydrophobic BAs including deoxycholate (DCA), taurocholate (TCA), taurochenodeoxycholate (TCDCA), and taurolithocholate (TLCA) were substantially increased in a streptozotocin and high fat diet (HFD) induced nonalcoholic steatohepatitis-hepatocellular carcinoma (NASH-HCC) mouse model. Additionally chronic HFD-fed mice spontaneously developed liver tumors with significantly increased hepatic BA levels. Enhancing intestinal excretion of hydrophobic BAs in the NASH-HCC model mice by a 2% cholestyramine feeding significantly prevented HCC development. The gut microbiota alterations were closely correlated with altered BA levels in liver and feces. HFD-induced inflammation inhibited key BA transporters, resulting in sustained increases in intrahepatic BA concentrations. Our study also showed a significantly increased cell proliferation in BA treated normal human hepatic cell lines and a down-regulated expression of tumor suppressor gene CEBPα in TCDCA treated HepG2 cell line, suggesting that several hydrophobic BAs may collaboratively promote liver carcinogenesis.
Persistent Identifierhttp://hdl.handle.net/10722/342525
ISSN
2023 Impact Factor: 5.7
2023 SCImago Journal Rankings: 2.131
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorXie, Guoxiang-
dc.contributor.authorWang, Xiaoning-
dc.contributor.authorHuang, Fengjie-
dc.contributor.authorZhao, Aihua-
dc.contributor.authorChen, Wenlian-
dc.contributor.authorYan, Jingyu-
dc.contributor.authorZhang, Yunjing-
dc.contributor.authorLei, Sha-
dc.contributor.authorGe, Kun-
dc.contributor.authorZheng, Xiaojiao-
dc.contributor.authorLiu, Jiajian-
dc.contributor.authorSu, Mingming-
dc.contributor.authorLiu, Ping-
dc.contributor.authorJia, Wei-
dc.date.accessioned2024-04-17T07:04:26Z-
dc.date.available2024-04-17T07:04:26Z-
dc.date.issued2016-
dc.identifier.citationInternational Journal of Cancer, 2016, v. 139, n. 8, p. 1764-1775-
dc.identifier.issn0020-7136-
dc.identifier.urihttp://hdl.handle.net/10722/342525-
dc.description.abstractDysregulated bile acids (BAs) are closely associated with liver diseases and attributed to altered gut microbiota. Here, we show that the intrahepatic retention of hydrophobic BAs including deoxycholate (DCA), taurocholate (TCA), taurochenodeoxycholate (TCDCA), and taurolithocholate (TLCA) were substantially increased in a streptozotocin and high fat diet (HFD) induced nonalcoholic steatohepatitis-hepatocellular carcinoma (NASH-HCC) mouse model. Additionally chronic HFD-fed mice spontaneously developed liver tumors with significantly increased hepatic BA levels. Enhancing intestinal excretion of hydrophobic BAs in the NASH-HCC model mice by a 2% cholestyramine feeding significantly prevented HCC development. The gut microbiota alterations were closely correlated with altered BA levels in liver and feces. HFD-induced inflammation inhibited key BA transporters, resulting in sustained increases in intrahepatic BA concentrations. Our study also showed a significantly increased cell proliferation in BA treated normal human hepatic cell lines and a down-regulated expression of tumor suppressor gene CEBPα in TCDCA treated HepG2 cell line, suggesting that several hydrophobic BAs may collaboratively promote liver carcinogenesis.-
dc.languageeng-
dc.relation.ispartofInternational Journal of Cancer-
dc.subjectbile acids-
dc.subjectgut microbiota-
dc.subjectinflammation-
dc.subjectliver carcinogenesis-
dc.subjectproliferation-
dc.titleDysregulated hepatic bile acids collaboratively promote liver carcinogenesis-
dc.typeArticle-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1002/ijc.30219-
dc.identifier.pmid27273788-
dc.identifier.scopuseid_2-s2.0-84981156450-
dc.identifier.volume139-
dc.identifier.issue8-
dc.identifier.spage1764-
dc.identifier.epage1775-
dc.identifier.eissn1097-0215-
dc.identifier.isiWOS:000383284500011-

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