ArticleJournal of virology2011
Hepatitis B virus X protein enhances cisplatin-induced hepatotoxicity via a mechanism involving degradation of Mcl-1.
Article in Journal of virology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 29 citations in OpenAlex.
- The interplay between hepatitis B virus and antitumor drugs in the treatment of hepatocellular carcinoma.Clinical and experimental medicine · 2025Review
- Article
- Mcl-1 Protein and Viral Infections: A Narrative Review.International journal of molecular sciences · 2024Review
- Screening of the HBx transactivation domain interacting proteins and the function of interactor Pin1 in HBV replication.Scientific reports · 2021Article
- Possible protective activity of n-acetyl cysteine against cisplatin‑induced hepatotoxicity in rats.Molecular biology reports · 2021Article
- MicroRNA‑186‑5p mediates osteoblastic differentiation and cell viability by targeting CXCL13 in non‑traumatic osteonecrosis.Molecular medicine reports · 2019Article
- Host transcription factor Speckled 110 kDa (Sp110), a nuclear body protein, is hijacked by hepatitis B virus protein X for viral persistence.The Journal of biological chemistry · 2017Article
- Upregulate KIF4A Enhances Proliferation, Invasion of Hepatocellular Carcinoma and Indicates poor prognosis Across Human Cancer Types.Scientific reports · 2017Article
- Article
- Overexpression of CHKA contributes to tumor progression and metastasis and predicts poor prognosis in colorectal carcinoma.Oncotarget · 2016Article
- Hepatocyte Factor JMJD5 Regulates Hepatitis B Virus Replication through Interaction with HBx.Journal of virology · 2016Article
- Upregulation of NETO2 expression correlates with tumor progression and poor prognosis in colorectal carcinoma.BMC cancer · 2015Article
- Overexpression of SULT2B1b is an independent prognostic indicator and promotes cell growth and invasion in colorectal carcinoma.Laboratory investigation; a journal of technical methods and pathology · 2015Article
- Oxidative stress in alcoholic and viral hepatitis.North American journal of medical sciences · 2012Article
- Viral product trafficking to mitochondria, mechanisms and roles in pathogenesis.Infectious disorders drug targets · 2012Review
- Article
- HBx sensitizes cells to oxidative stress-induced apoptosis by accelerating the loss of Mcl-1 protein via caspase-3 cascade.Molecular cancer · 2011Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatitis B virus X protein (HBx) is implicated in the pathogenesis of hepatitis B virus (HBV)-associated liver diseases. However, whether HBx has the ability to disturb the susceptibility of hepatocytes to common chemotherapeutic agents remains incompletely understood. Here we demonstrate that HBx enhances cisplatin-induced hepatotoxicity by a mechanism involving degradation of Mcl-1, an antiapoptotic member of the Bcl-2 family. Ectopic expression of HBx sensitized hepatocytes to cisplatin-induced apoptosis, which was accompanied by a marked downregulation of Mcl-1 but not of Bcl-2 or Bcl-xL. Overexpression of Mcl-1 prevented HBx-induced proapoptotic and proinflammatory effects during cisplatin treatment both in vitro and in vivo. HBx-induced dysregulation of Mcl-1 resulted mainly from posttranslational degradation rather than transcription repression. Moreover, a caspase-3 inhibitor effectively abrogated HBx-enhanced Mcl-1 degradation and cell death. Importantly, antioxidants blocked activation of caspase-3 and acceleration of Mcl-1 loss, as well as cell death, in HBx-expressing hepatocytes upon cisplatin exposure in vitro and in vivo. Collectively, these data implicate oxidative stress-dependent caspase-3-mediated degradation of Mcl-1 as a mechanism contributing to HBx-mediated sensitization of cisplatin-induced hepatotoxicity. A combination of cisplatin and antioxidants might provide more advantage than cisplatin alone in the treatment of cancer patients with chronic HBV infection.
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