ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2013
Mechanisms of STAT3 activation in the liver of FXR knockout mice.
Article in American journal of physiology. Gastrointestinal and liver physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 31 citations in OpenAlex.
- Dietary Supplementation of Glutamate Alleviates LPS-Induced Intestinal Injury Associated with mAnimals : an open access journal from MDPI · 2026Article
- Effects of therapeutically approved individual bile acids on the development of metabolic dysfunction-associated steatohepatitis a low bile acid mouse model.Toxicological sciences : an official journal of the Society of Toxicology · 2024Article
- Gut Microbiota, Deranged Immunity, and Hepatocellular Carcinoma.Biomedicines · 2024Review
- Current Perspectives on the Molecular and Clinical Relationships between Primary Biliary Cholangitis and Hepatocellular Carcinoma.International journal of molecular sciences · 2024Review
- Unveiling the complex relationship between gut microbiota and liver cancer: opportunities for novel therapeutic interventions.Gut microbes · 2023Review
- Pleiotropic roles of FXR in liver and colorectal cancers.Molecular and cellular endocrinology · 2022Article
- Farnesoid X receptor activation induces antitumour activity in colorectal cancer by suppressing JAK2/STAT3 signalling via transactivation of SOCS3 gene.Journal of cellular and molecular medicine · 2020Article
- The FXR Agonist, Obeticholic Acid, Suppresses HCC Proliferation & Metastasis: Role of IL-6/STAT3 Signalling Pathway.Scientific reports · 2017Article
- Long-term Administration of Nuclear Bile Acid Receptor FXR Agonist Prevents Spontaneous Hepatocarcinogenesis in Abcb4Scientific reports · 2017Article
- SOCS1 regulates hepatic regenerative response and provides prognostic makers for acute obstructive cholangitis.Scientific reports · 2017Article
- Long noncoding RNA MEG3 induces cholestatic liver injury by interaction with PTBP1 to facilitate shp mRNA decay.Hepatology (Baltimore, Md.) · 2017Article
- Bile acids promote diethylnitrosamine-induced hepatocellular carcinoma via increased inflammatory signaling.American journal of physiology. Gastrointestinal and liver physiology · 2016Article
- Mice with hepatocyte-specific FXR deficiency are resistant to spontaneous but susceptible to cholic acid-induced hepatocarcinogenesis.American journal of physiology. Gastrointestinal and liver physiology · 2016Article
- Activated FXR Inhibits Leptin Signaling and Counteracts Tumor-promoting Activities of Cancer-Associated Fibroblasts in Breast Malignancy.Scientific reports · 2016Article
- Nuclear bile acid signaling through the farnesoid X receptor.Cellular and molecular life sciences : CMLS · 2015Review
- Interactions Between Nuclear Receptor SHP and FOXA1 Maintain Oscillatory Homocysteine Homeostasis in Mice.Gastroenterology · 2015Article
- FXR and liver carcinogenesis.Acta pharmacologica Sinica · 2015Review
- Bile acid dysregulation, gut dysbiosis, and gastrointestinal cancer.Experimental biology and medicine (Maywood, N.J.) · 2014Review
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Authors and funding
10 authors at 6 institutions in 2 countries.
Funding
Abstract
Farnesoid X receptor (FXR, Nr1h4) is a ligand-activated transcription factor belonging to the nuclear receptor superfamily. FXR is essential in maintaining bile acid (BA) homeostasis, and FXR(-/-) mice develop cholestasis, inflammation, and spontaneous liver tumors. The signal transducer and activator of transcription 3 (STAT3) is well known to regulate liver growth, and STAT3 is feedback inhibited by its target gene, the suppressor of cytokine signaling 3 (SOCS3). Strong activation of STAT3 was detected in FXR(-/-) mouse livers. However, the mechanism of STAT3 activation with FXR deficiency remains elusive. Wild-type (WT) and FXR(-/-) mice were used to detect STAT3 pathway activation in the liver. In vivo BA feeding or deprivation was used to determine the role of BAs in STAT3 activation, and in vitro molecular approaches were used to determine the direct transcriptional regulation of SOCS3 by FXR. STAT3 was activated in FXR(-/-) but not WT mice. BA feeding increased, but deprivation by cholestyramine reduced, serum inflammatory markers and STAT3 activation. Furthermore, the Socs3 gene was determined as a direct FXR target gene. The elevated BAs and inflammation, along with reduced SOCS3, collectively contribute to the activation of the STAT3 signaling pathway in the liver of FXR(-/-) mice. This study suggests that the constitutive activation of STAT3 may be a mechanism of liver carcinogenesis in FXR(-/-) mice.
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