NDLI: The deficiency of G-protein-coupled bile acid receptor Gpbar1 (TGR5) enhances chemically-induced liver carcinogenesis

Content Provider	PubMed Central
Author	Chen, Wei-dong Donna, Yu Forman, Barry M. Huang, Wendong Wang, Yan-dong
Abstract	Gpbar1 (TGR5), a membrane-bound bile acid receptor, is well known for its roles in regulation of energy homeostasis and glucose metabolism. We recently reported that TGR5 activation inhibits nuclear factor κB (NF-κB)-mediated inflammation. Here we show that TGR5 deficiency enhances chemically-induced liver carcinogenesis, and that TGR5 is a negative regulator of signal transducer and activator of transcription 3 (STAT3) signaling. Mice lacking TGR5 were much more susceptible to diethylnitrosamine (DEN)-induced acute liver injury and liver carcinogenesis than wild-type (WT) mice. Consistent with the increasing incidence of liver cancer in TGR5−/− mice, hepatocyte death, compensatory proliferation, and gene expression of certain inflammatory cytokines and matrix metalloproteinases were more sensitive to DEN induction in the absence of TGR5 signaling. In vitro, TGR5 activation greatly inhibited proliferation and migration of human liver cancer cells. We then found that TGR5 activation strongly suppressed STAT3 signaling in vitro and in vivo. Furthermore, we revealed that TGR5 antagonizes STAT3 pathway through suppressing STAT3 phosphorylation, its transcription activity and DNA binding activity, which suggests that TGR5 antagonizes liver tumorigenesis at least in part by inhibiting STAT3 signaling.
Related Links	http://dx.doi.org/10.1002/hep.26019
Ending Page	666
Page Count	11
Starting Page	656
File Format	PDF
ISSN	02709139
e-ISSN	15273350
Journal	Hepatology (Baltimore, Md.)
Issue Number	2
Volume Number	57
Language	English
Publisher Date	2013-02-01
Access Restriction	Open
Subject Keyword	Medicine(all) Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Hepatology

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Retraction Statement: The Deficiency of G-Protein-Coupled Bile Acid Receptor Gpbar1 (TGR5) Enhances Chemically-Induced Liver Carcinogenesis

The deficiency of G-protein-coupled bile acid receptor Gpbar1 (TGR5) enhances chemically-induced liver carcinogenesis. : Retraction

Deficiency of G-protein-coupled bile acid receptor Gpbar1 (TGR5) enhances chemically induced liver carcinogenesis.

The G-protein coupled bile acid receptor Gpbar1 (TGR5) negatively regulates hepatic inflammatory response through antagonizing Nuclear Factor κB

Aberrant DNA Methylation of G-protein-coupled Bile Acid Receptor Gpbar1 (TGR5) is a Potential Biomarker for Hepatitis B Virus Associated Hepatocellular Carcinoma

The G-Protein-Coupled Bile Acid Receptor Gpbar1 (TGR5) Inhibits Gastric Inflammation Through Antagonizing NF-κB Signaling Pathway

The G-Protein-Coupled Bile Acid Receptor Gpbar1 (TGR5) Inhibits Gastric Inflammation Through Antagonizing NF-κB Signaling Pathway

Bile acids and liver carcinogenesis: TGR5 as a novel piece in the puzzle?

The G-protein-coupled bile acid receptor Gpbar1 (TGR5) suppresses gastric cancer cell proliferation and migration through antagonizing STAT3 signaling pathway

The deficiency of G-protein-coupled bile acid receptor Gpbar1 (TGR5) enhances chemically-induced liver carcinogenesis

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Retraction Statement: The Deficiency of G-Protein-Coupled Bile Acid Receptor Gpbar1 (TGR5) Enhances Chemically-Induced Liver Carcinogenesis

The deficiency of G-protein-coupled bile acid receptor Gpbar1 (TGR5) enhances chemically-induced liver carcinogenesis. : Retraction

Deficiency of G-protein-coupled bile acid receptor Gpbar1 (TGR5) enhances chemically induced liver carcinogenesis.

The G-protein coupled bile acid receptor Gpbar1 (TGR5) negatively regulates hepatic inflammatory response through antagonizing Nuclear Factor κB

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