Journal
WORLD JOURNAL OF GASTROENTEROLOGY
Volume 22, Issue 17, Pages 4345-4353Publisher
BAISHIDENG PUBLISHING GROUP INC
DOI: 10.3748/wjg.v22.i17.4345
Keywords
Hepatitis B virus; Reactive oxygen species; Apoptosis; Manganese superoxide dismutase; AMP-activated protein kinase
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Funding
- National Nature Science Foundation of China [81400639, 81502507]
- Doctoral Start-up Foundation of Guangzhou Medical University of China [2014C39]
- Science Foundation for Youth Scientists of the Second People's Hospital of Guangdong Province of China [YQ2015-002]
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AIM: To investigate the anti-apoptotic capability of the hepatitis B virus (HBV) in the HepG2 hepatoma cell line and the underlying mechanisms. METHODS: Cell viability and apoptosis were measured by MTT assay and flow cytometry, respectively. Targeted knockdown of manganese superoxide dismutase (MnSOD), AMP-activated protein kinase (AMPK) and hepatitis B virus X protein (HBx) genes as well as AMPK agonist AICAR and antagonist compound C were employed to determine the correlations of expression of these genes. RESULTS: HBV markedly protected the hepatoma cells from growth suppression and cell death in the condition of serum deprivation. A decrease of superoxide anion production accompanied with an increase of MnSOD expression and activity was found in HepG2.215 cells. Moreover, AMPK activation contributed to the up-regulation of MnSOD. HBx protein was identified to induce the expression of AMPK and MnSOD. CONCLUSION: Our results suggest that HBV suppresses mitochondrial superoxide level and exerts an antiapoptotic effect by activating AMPK/MnSOD signaling pathway, which may provide a novel pharmacological strategy to prevent HCC.
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