AI Article Synopsis
- Chenodeoxycholic acid (CDCA) and synthetic FXR agonist GW4064 were found to significantly boost the expression of the tumor suppressor NDRG2 in human liver cancer cells and primary hepatocytes.
- Knockdown of FXR eliminated this induction from CDCA, indicating that FXR is crucial for this process, while overexpressing a more active FXR variant led to increased NDRG2 levels.
- Additionally, the study identified a specific FXR-response element in the DNA of both human and mouse genes, suggesting a potential link between bile acids, metabolism, and cancer biology.
Article Abstract
Here we report that bile acid chenodeoxycholic acid (CDCA) and synthetic farnesoid X receptor (FXR) agonist GW4064 robustly induced tumor suppressor N-Myc downstream regulated gene 2 (NDRG2) expression in human hepatoma cells and primary hepatocytes. Knockdown of FXR abolished the induction by CDCA, whereas overexpression of a constitutively active form of FXR increased NDRG2 expression. A FXR-response element was identified within intronic regions of human and murine genes. Moreover, mice given GW4064 exhibit an increase of Ndrg2 expression in liver and kidney, where both NDRG2 and FXR are enriched. The identification of NDRG2 as a bile acid regulated gene may provide novel knowledge toward the understanding of NDRG2 physiological function and the link between metabolism and cancer.
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| http://dx.doi.org/10.1016/j.bbrc.2013.03.058 | DOI Listing |
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