ArticleMolecular cancer2011
HBx sensitizes cells to oxidative stress-induced apoptosis by accelerating the loss of Mcl-1 protein via caspase-3 cascade.
Article in Molecular cancer, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 60 citations in OpenAlex.
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- Sulforaphane alleviates lung ischemia‑reperfusion injury through activating Nrf‑2/HO‑1 signaling.Experimental and therapeutic medicine · 2023Article
- Role of hepatitis B virus non-structural protein HBx on HBV replication, interferon signaling, and hepatocarcinogenesis.Frontiers in microbiology · 2023Review
- Allicin protects against renal ischemia-reperfusion injury by attenuating oxidative stress and apoptosis.International urology and nephrology · 2022Article
- Genome-Wide Association Study for Chronic Hepatitis B Infection in the Thai Population.Frontiers in genetics · 2022Article
- Inhibition of Protease Activated Receptor 2 Attenuates HBx-Induced Inflammation and Mitochondria Oxidative Stress.Infection and drug resistance · 2022Article
- Effect of oxidative stress and calcium deregulation on FAM26F (CALHM6) expression during hepatitis B virus infection.BMC infectious diseases · 2021Article
- Human neurotropic polyomavirus, JC virus, agnoprotein targets mitochondrion and modulates its functions.Virology · 2021Article
- AnFrontiers in genetics · 2021Article
- Hepatocellular carcinoma (HCC): Epidemiology, etiology and molecular classification.Advances in cancer research · 2021Review
- Hepatitis B virus X protein promotes liver cell pyroptosis under oxidative stress through NLRP3 inflammasome activation.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2020Article
- Article
- Mitochondrial damage in hippocampal neurons of rats with epileptic protein expression of Fas and caspase-3.Experimental and therapeutic medicine · 2018Article
- Interference of Apoptosis by Hepatitis B Virus.Viruses · 2017Review
- Down-regulation of miR-146b-5p by long noncoding RNA MALAT1 in hepatocellular carcinoma promotes cancer growth and metastasis.Oncotarget · 2017Article
- Oxidative stress, a trigger of hepatitis C and B virus-induced liver carcinogenesis.Oncotarget · 2017Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundOxidative stress has been implicated in the pathogenesis of a wide spectrum of human diseases, including Hepatitis B virus (HBV)-related liver disease. Hepatitis B virus X protein (HBx) is a key regulator of HBV that exerts pleiotropic activity on cellular functions. Recent studies showed that HBx alters mitochondrial membrane potential, thereby sensitizing cells to pro-apoptotic signals. However, it remains largely unknown whether susceptibility of hepatocytes could be disturbed by HBx under oxidative stress conditions. The purpose of this study is to determine the apoptotic susceptibility of HBx-expressing hepatocytes upon exposure to pro-oxidant stimuli in vitro and in vivo and explore its underlying mechanism.
resultsAlthough expression of HBx itself did not activate apoptotic signaling, it significantly enhanced oxidative stress-induced cell death both in vitro and in vivo. Interestingly, this phenomenon was associated with a pronounced reduction of protein levels of Mcl-1, but not other anti-apoptotic Bcl-2 members. Importantly, enforced expression of Mcl-1 prevented HBx-triggered cell apoptosis; conversely, specific knockdown of Mcl-1 exacerbated HBx-induced apoptosis upon exposure to oxidative stress. Furthermore, inhibition of caspase-3 not only abrogated HBx-triggered apoptotic killing but also blocked HBx-induced Mcl-1 loss. Additionally, expression of HBx and Mcl-1 was found to be inversely correlated in HBV-related hepatocellular carcinogenesis (HCC) tissues.
conclusionsOur findings indicate that HBx exerts pro-apoptotic effect upon exposure to oxidative stress probably through accelerating the loss of Mcl-1 protein via caspase-3 cascade, which may shed a new light on the molecular mechanism of HBV-related hepatocarcinogenesis.
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