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The transcriptional activity of Gli1 is negatively regulated by AMPK through Hedgehog partial agonism in hepatocellular carcinoma

  • Authors:
    • Qiuran Xu
    • Xin Liu
    • Xin Zheng
    • Yingmin Yao
    • Maode Wang
    • Qingguang Liu
  • View Affiliations / Copyright

    Affiliations: Department of Hepatobiliary Surgery, The First Affiliated Hospital of Medical College of Xi'an Jiaotong University, Xi'an, Shaanxi 710061, P.R. China, Department of Neurosurgery, The First Affiliated Hospital of Medical College of Xi'an Jiaotong University, Xi'an, Shaanxi 710061, P.R. China
    Copyright: © Xu et al. This is an open access article distributed under the terms of Creative Commons Attribution License [CC BY_NC 3.0].
  • Pages: 733-741
    |
    Published online on: July 10, 2014
       https://doi.org/10.3892/ijmm.2014.1847
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Abstract

The aberrant activation of the Hedgehog (Hh) signaling pathway has been implicated in a variety of malignancies, including hepatocellular carcinoma (HCC). The mammalian 5' adenosine monophosphate-activated protein kinase (AMPK) plays a crucial role in cellular energy homeostasis. However, the interaction between the Hh and AMPK signaling pathways has not been investigated to date. In the present study, to the best of our knowlege, we report for the first time the negative regulation of glioma-associated oncogene 1 (Gli1), an important downstream effector of Hh, by the AMPK signal transduction pathway. Immunoprecipitation and GST-pull down assay showed a direct interaction between AMPK and Gli1. The overexpression of AMPK induced the downregulation of Gli1 expression, while the knockdown of AMPK upregulated Gli1 expression in a relatively short period of time (24 h or less). Our data suggest that AMPK may function as an upstream molecule that regulates Gli1 expression. Therefore, AMPK may play a role in the Hh signaling pathway, through which it regulates tumorigenesis.
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Copy and paste a formatted citation
Spandidos Publications style
Xu Q, Liu X, Zheng X, Yao Y, Wang M and Liu Q: The transcriptional activity of Gli1 is negatively regulated by AMPK through Hedgehog partial agonism in hepatocellular carcinoma. Int J Mol Med 34: 733-741, 2014.
APA
Xu, Q., Liu, X., Zheng, X., Yao, Y., Wang, M., & Liu, Q. (2014). The transcriptional activity of Gli1 is negatively regulated by AMPK through Hedgehog partial agonism in hepatocellular carcinoma. International Journal of Molecular Medicine, 34, 733-741. https://doi.org/10.3892/ijmm.2014.1847
MLA
Xu, Q., Liu, X., Zheng, X., Yao, Y., Wang, M., Liu, Q."The transcriptional activity of Gli1 is negatively regulated by AMPK through Hedgehog partial agonism in hepatocellular carcinoma". International Journal of Molecular Medicine 34.3 (2014): 733-741.
Chicago
Xu, Q., Liu, X., Zheng, X., Yao, Y., Wang, M., Liu, Q."The transcriptional activity of Gli1 is negatively regulated by AMPK through Hedgehog partial agonism in hepatocellular carcinoma". International Journal of Molecular Medicine 34, no. 3 (2014): 733-741. https://doi.org/10.3892/ijmm.2014.1847
Copy and paste a formatted citation
x
Spandidos Publications style
Xu Q, Liu X, Zheng X, Yao Y, Wang M and Liu Q: The transcriptional activity of Gli1 is negatively regulated by AMPK through Hedgehog partial agonism in hepatocellular carcinoma. Int J Mol Med 34: 733-741, 2014.
APA
Xu, Q., Liu, X., Zheng, X., Yao, Y., Wang, M., & Liu, Q. (2014). The transcriptional activity of Gli1 is negatively regulated by AMPK through Hedgehog partial agonism in hepatocellular carcinoma. International Journal of Molecular Medicine, 34, 733-741. https://doi.org/10.3892/ijmm.2014.1847
MLA
Xu, Q., Liu, X., Zheng, X., Yao, Y., Wang, M., Liu, Q."The transcriptional activity of Gli1 is negatively regulated by AMPK through Hedgehog partial agonism in hepatocellular carcinoma". International Journal of Molecular Medicine 34.3 (2014): 733-741.
Chicago
Xu, Q., Liu, X., Zheng, X., Yao, Y., Wang, M., Liu, Q."The transcriptional activity of Gli1 is negatively regulated by AMPK through Hedgehog partial agonism in hepatocellular carcinoma". International Journal of Molecular Medicine 34, no. 3 (2014): 733-741. https://doi.org/10.3892/ijmm.2014.1847
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