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Regulation of AKR1B1 by thyroid hormone and its receptors.

Authors: Liao, CS  Tai, PJ  Huang, YH  Chen, RN  Wu, SM  Kuo, LW  Yeh, CT  Tsai, MM  Chen, WJ  Lin, KH 
Citation: Liao CS, etal., Mol Cell Endocrinol. 2009 Aug 13;307(1-2):109-17. doi: 10.1016/j.mce.2009.04.013. Epub 2009 May 5.
Pubmed: (View Article at PubMed) PMID:19422879
DOI: Full-text: DOI:10.1016/j.mce.2009.04.013

The objective of this study was to identify genes regulated by thyroid hormone (T(3)) mediated by its receptor (TR) and associated with tumorigenesis. The gene encoding aldo-keto reductase family 1, member B1 (AKR1B1), as previously identified by c-DNA microarray, is known to be up-regulated by T(3) treatment. Enzyme AKR1B1 was elevated roughly 3-fold in HepG2-TRalpha1 cells at the protein level and 4.6-fold increase at the mRNA level after 48 h T(3) treatment. Similar findings were obtained from thyroidectomized rats after T(3) application. To identify and localize the critical TR element (TRE), series deletion of the promoter mutant were constructed and electrophoretic mobility shift assays were carried out. The TRE on the AKR1B1 promoter was localized to the -1099/-1028 region. Further, this study demonstrated that AKR1B1 over-expression in some types of hepatocellular carcinomas (HCCs) is TR-dependent and might play a crucial role in the development of HCC. Thus, T(3) regulates AKR1B1 gene expression via a TRE-dependant mechanism and associates liver cancer.


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RGD Object Information
RGD ID: 8548685
Created: 2014-03-19
Species: All species
Last Modified: 2014-03-19
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.