Hepatitis B virus X (HBX) protein upregulates β-catenin in a human hepatic cell line by sequestering SIRT1 deacetylase

Srisuttee,Ratakorn; Koh,Sang  Seok; Kim,Su  Jin; Malilas,Waraporn; Boonying,Wassamon; Cho,Il-Rae; Jhun,Byung  Hak; Ito,Masafumi; Horio,Yoshiyuki; Seto,Edward; Oh,Sangtaek; Chung,Young-Hwa

doi:10.3892/or.2012.1798

July 2012 Volume 28 Issue 1

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July 2012 Volume 28 Issue 1

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Article

Hepatitis B virus X (HBX) protein upregulates β-catenin in a human hepatic cell line by sequestering SIRT1 deacetylase

Authors:
- Ratakorn Srisuttee
- Sang Seok Koh
- Su Jin Kim
- Waraporn Malilas
- Wassamon Boonying
- Il-Rae Cho
- Byung Hak Jhun
- Masafumi Ito
- Yoshiyuki Horio
- Edward Seto
- Sangtaek Oh
- Young-Hwa Chung
View Affiliations / Copyright

Affiliations: WCU, Department of Cogno-Mechatronics Engineering, Pusan National University, Busan, Republic of Korea, Immunotherapy Research Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon, Republic of Korea, Department of Nanomedical Engineering, Pusan National University, Busan, Republic of Korea, Department of Urology, Gifu University Graduate School of Medicine, Gifu, Japan, Department of Pharmacology, Sapporo Medical University, Sapporo, Japan, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL, USA, Department of Advanced Fermentation Fusion Science and Technology, Kookmin University, Seoul, Republic of Korea
Pages: 276-282
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Published online on: May 4, 2012

https://doi.org/10.3892/or.2012.1798
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Abstract

Hepatitis B virus X (HBX) protein has been reported to induce upregulation of β-catenin, a known proto-oncogene, in p53-knockout and p53-mutant hepatic cell lines both in a GSK-3β-dependent manner and via interaction with adenomatous polyposis coli, which results in protection from β-catenin degradation. In this study, we describe a novel mechanism for HBX-mediated upregulation of β-catenin. We observed that HBX interacts with SIRT1, a class III histone deacetylase. Furthermore, the presence of HBX attenuated the interaction between SIRT1 and β-catenin, leading to protection of β-catenin from the inhibitory action of SIRT1. Reduction of SIRT1 with siRNA or suppression of SIRT1 activity with nicotinamide upregulated β-catenin protein levels. In contrast, enhancement of SIRT1 activity with resveratrol reduced β-catenin protein levels. Furthermore, in Hep3B cells stably expressing HBX, overexpression of SIRT1 or treatment with resveratrol enhanced sensitivity to doxorubicin-induced apoptosis, indicating that upregulation of SIRT1 could be a therapeutic strategy for HBV-related hepatocellular carcinoma. Based on these results, we propose that HBX upregulates β-catenin by sequestering SIRT1, which leads to anticancer drug treatment resistance.

Journals

International Journal of Molecular Medicine

International Journal of Oncology

Molecular Medicine Reports

Oncology Reports

Experimental and Therapeutic Medicine

Oncology Letters

Biomedical Reports

Molecular and Clinical Oncology

World Academy of Sciences Journal

International Journal of Functional Nutrition

International Journal of Epigenetics

Medicine International

Hepatitis B virus X (HBX) protein upregulates β-catenin in a human hepatic cell line by sequestering SIRT1 deacetylase

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