ArticleWorld journal of gastroenterology2010
HBx-induced reactive oxygen species activates hepatocellular carcinogenesis via dysregulation of PTEN/Akt pathway.
Article in World journal of gastroenterology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 64 citations in OpenAlex.
- Hepatitis B-Induced Hepatocellular Carcinoma: Understanding Viral Carcinogenesis and Disease Management.Journal of clinical medicine · 2025Review
- Insight into the mechanisms regulating liver cancer stem cells by hepatitis B virus X protein.Infectious agents and cancer · 2024Review
- Protective effect of N-acetylcysteine against hepatocellular carcinoma in hepatitis B virus carriers.American journal of cancer research · 2024Article
- The Role of PI3K/AKT/mTOR Signaling in Hepatocellular Carcinoma Metabolism.International journal of molecular sciences · 2023Review
- Atorvastatin favorably modulates a clinical hepatocellular carcinoma risk gene signature.Hepatology communications · 2022Article
- The HBx protein from hepatitis B virus coordinates a redox-active Fe-S cluster.The Journal of biological chemistry · 2022Article
- Antioxidant Role of Kaempferol in Prevention of Hepatocellular Carcinoma.Antioxidants (Basel, Switzerland) · 2021Review
- Spatiotemporal regulation of hydrogen sulfide signaling in the kidney.Redox biology · 2021Review
- Phosphatase and Tensin Homolog in Non-neoplastic Digestive Disease: More Than Just Tumor Suppressor.Frontiers in physiology · 2021Review
- The Mechanisms of HBV-Induced Hepatocellular Carcinoma.Journal of hepatocellular carcinoma · 2021Review
- Effect of HBx on inflammation and mitochondrial oxidative stress in mouse hepatocytes.Oncology letters · 2020Article
- Role of alcohol in pathogenesis of hepatitis B virus infection.World journal of gastroenterology · 2020Review
- Peroxiredoxin 5 ameliorates obesity-induced non-alcoholic fatty liver disease through the regulation of oxidative stress and AMP-activated protein kinase signaling.Redox biology · 2020Article
- Relevance of reactive oxygen species in liver disease observed in transgenic mice expressing the hepatitis B virus X protein.Laboratory animal research · 2020Review
- Nanocarrier-mediated antioxidant delivery for liver diseases.Theranostics · 2020Review
- Adaptive Responses to Electrophilic Stress and Reactive Sulfur Species as their Regulator Molecules.Toxicological research · 2019Review
- Serum anti-EIF3A autoantibody as a potential diagnostic marker for hepatocellular carcinoma.Scientific reports · 2019Article
- Peroxiredoxin 1, a Novel HBx-Interacting Protein, Interacts with Exosome Component 5 and Negatively Regulates Hepatitis B Virus (HBV) Propagation through Degradation of HBV RNA.Journal of virology · 2019Article
- Identification of anti-SF3B1 autoantibody as a diagnostic marker in patients with hepatocellular carcinoma.Journal of translational medicine · 2018Article
- Reactive Oxygen Species-Mediated c-Jun NHJournal of virology · 2017Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimTo 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.
methodsCell 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 FACScalibur. Identification of oxidized and reduced phosphatase and tensin homolog (PTEN) was analyzed through N-ethylmaleimide alkylation, nonreducing electrophoresis.
resultsWe 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.
conclusionHBx induced ROS promoted Akt pathways via oxidized inactive PTEN. HBx and ROS maintained a positive regulatory loop, which aggravated carcinogenesis.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.