SIRT1 sensitizes hepatocellular carcinoma cells expressing hepatitis B virus X protein to oxidative stress-induced apoptosis

Srisuttee, Ratakorn; Koh, Sang Seok; Malilas, Waraporn; Moon, Jeong; Cho, Il-Rae; Jhun, Byung Hak; Horio, Yoshiyuki; Chung, Young‐Hwa

doi:10.1016/j.bbrc.2012.10.102

Cited by 20 publications

(19 citation statements)

References 32 publications

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“…Although HBV (HBx)-triggered oxidative stress may lead to cell death [269, 330], solid data have been accumulated suggesting that HBV can also confer protection against exogenous ROS, such as hydrogen peroxide [331–334]. This is achieved by several routes, including (i) activation of the Nrf2/ARE pathway [287] and subsequent induction or augmentation of expression of liver regeneration (ALR) protein [335]; (ii) hypermethylation of the p16 INK4a promoter, leading to alterations in the induction of a senescence p16 INK4a regulator with subsequent prevention of cell cycle arrest [332]; and (iii) induction of the forkhead transcription factor FOXO4 [333].…”

Section: Hepatitis C Virusmentioning

confidence: 99%

Oxidative stress, a trigger of hepatitis C and B virus-induced liver carcinogenesis

et al. 2016

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Virally induced liver cancer usually evolves over long periods of time in the context of a strongly oxidative microenvironment, characterized by chronic liver inflammation and regeneration processes. They ultimately lead to oncogenic mutations in many cellular signaling cascades that drive cell growth and proliferation. Oxidative stress, induced by hepatitis viruses, therefore is one of the factors that drives the neoplastic transformation process in the liver. This review summarizes current knowledge on oxidative stress and oxidative stress responses induced by human hepatitis B and C viruses. It focuses on the molecular mechanisms by which these viruses activate cellular enzymes/systems that generate or scavenge reactive oxygen species (ROS) and control cellular redox homeostasis. The impact of an altered cellular redox homeostasis on the initiation and establishment of chronic viral infection, as well as on the course and outcome of liver fibrosis and hepatocarcinogenesis will be discussed The review neither discusses reactive nitrogen species, although their metabolism is interferes with that of ROS, nor antioxidants as potential therapeutic remedies against viral infections, both subjects meriting an independent review.

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Section: Hepatitis C Virusmentioning

confidence: 99%

Oxidative stress, a trigger of hepatitis C and B virus-induced liver carcinogenesis

et al. 2016

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“…The downregulation of p-STAT3 and p-AKT caused decrease of cyclinD1, VEGF and MMP-9 in this process. In Hep3B cells stably expressing hepatitis B virus (HBV) treated with resveratrol (100 μM), ectopic expression and enhanced activity of SIRT1 were seen, which attenuated JNK phosphorylation, a prerequisite for resistance to oxidative stress-induced apoptosis (61). On the other hand, some research indicated that resveratrol might not activate but inhibit SIRT1 signal in HepG2 cells.…”

Section: Role Of Sirt1 In Apoptosismentioning

confidence: 99%

Anti-tumor effects and cellular mechanisms of resveratrol

Han

Xia

Gao

et al. 2015

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“…Of these, the JNK pathway has been reported to be inhibited by sorafenib [6] and have a possibility to regulate HBV pathogenesis. [7] Therefore, we investigated if the JNK pathway is blocked by sorafenib and HBV gene expression is suppressed by JNK inhibition. As expected, phosphorylation of JNK and HBV protein levels were decreased by sorafenib [ Figure 2a].…”

Section: Sorafenib Suppresses Hbv Gene Expressionmentioning

confidence: 99%

Sorafenib suppresses hepatitis B virus gene expression via inhibiting JNK pathway

et al. 2015

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Aim: Hepatitis B virus (HBV) infection is a major cause of chronic liver diseases. Sorafenib is a multikinase inhibitor and an approved anti-liver cancer drug. Here we demonstrated the antiviral effect of sorafenib on HBV gene expression. Methods: To investigate the effect of sorafenib on HBV gene expression, a luciferase assay was performed with ×1.3 Cp-luciferase HBV construct and reverse transcriptase polymerase chain reaction (PCR), real-time PCR, and Western blotting analyses were performed using HepG2 cells derived from hepatocellular carcinoma and Chang liver cells derived from a normal liver tissue. Results: Sorafenib suppressed HBV gene expression via inhibiting the JNK pathway. In this process, the farnesoid X receptor (FXR), a transcription factor that has been reported to increase HBV replication and gene expression, was under control of the JNK pathway. Notably, JNK activation increased FXR protein levels, not mRNA levels. Conclusion: Sorafenib suppressed HBV gene expression via inhibiting the JNK pathway, which regulates FXR activity.

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SIRT1 sensitizes hepatocellular carcinoma cells expressing hepatitis B virus X protein to oxidative stress-induced apoptosis

Cited by 20 publications

References 32 publications

Oxidative stress, a trigger of hepatitis C and B virus-induced liver carcinogenesis

Oxidative stress, a trigger of hepatitis C and B virus-induced liver carcinogenesis

Anti-tumor effects and cellular mechanisms of resveratrol

Sorafenib suppresses hepatitis B virus gene expression via inhibiting JNK pathway

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