Journal
WORLD JOURNAL OF GASTROENTEROLOGY
Volume 16, Issue 39, Pages 4932-4937Publisher
BAISHIDENG PUBLISHING GROUP INC
DOI: 10.3748/wjg.v16.i39.4932
Keywords
Hepatitis B virus X protein; Hepatocellular carcinoma; Akt; Reactive oxygen species; Phosphatase and tensin homolog
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Funding
- 21st century Frontier Program in the Functional Human Genome Project [HGM0200934]
- International Collaboration Program of Science and Technology [FGM0600914]
- Ministry of Education, Science Technology [NBM3300711]
- KRIBB Research Initiative Program [KGM3320911]
- National Research Foundation of Korea [2007-00529, 2007-03792] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
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AIM: To investigate the role of hepatitis B virus X-protein (HBx)-induced reactive oxygen species (ROS) on liver carcinogenesis in HBx transgenic mice and HepG2-HBx cells. METHODS: Cell growth rate was analyzed, and through western blotting, mitogenic signaling was observed. Endogenous ROS from wild and HBx transgenic mice and HepG2-Mock and HBx cells were assayed by FACS-calibur. Identification of oxidized and reduced phosphatase and tensin homolog (PTEN) was analyzed through N-ethylmaleimide alkylation, nonreducing electrophoresis. RESULTS: We observed that the cell-proliferation-related phosphoinositide 3-kinase/Akt pathway is activated by HBx in vivo and in vitro. Increased ROS were detected by HBx. Tumor suppressor PTEN, via dephosphorylation of Akt, was oxidized and inactivated by increased ROS. Increased oxidized PTEN activated the mitogenic pathway through over-activated Akt. However, treatment with ROS scavenger N-acetyl cysteine can reverse PTEN to a reduced form. Endogenously produced ROS also stimulated HBx expression. CONCLUSION: HBx induced ROS promoted Akt pathways via oxidized inactive PTEN. HBx and ROS maintained a positive regulatory loop, which aggravated carcinogenesis. (C) 2010 Baishideng. All rights reserved.
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