Erratum to “Curcumin inhibits hepatitis B virus via down‐regulation of the metabolic coactivator PGC‐1α” [FEBS Lett. 584 (2010) 2485–2490]

Rechtman, Maya Mouler; Har-Noy, Ofir; Bar-Yishay, Iddo; Fishman, Sigal; Adamovich, Yaarit; Shaul, Yosef; Halpern, Zamir; Shlomai, Amir

doi:10.1016/j.febslet.2010.05.041

Cited by 18 publications

(26 citation statements)

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“…Its multiple-target characteristics influence several activities of intracellular molecules, including transcription nuclear factor-κB (NF-κB), pro-inflammatory cyclooxygenase-2 and MAPK inhibitions, as well as heme oxygenase-1 induction (9). In the antivirus bioactivity, certain reports have indicated that curcumin showed anti-viral activity against the human immunodeficiency (10,11), the coxsackie- (12) and the hepatitis B (HBV) viruses (13). In the anti-HCV study, one report showed that curcumin inhibited a lipogenic transcription factor, sterol regulatory element binding protein-1 (SREBP-1)-induced HCV replication via the inhibition of the PI3K-AKT pathway (14).…”

Section: Introductionmentioning

confidence: 99%

Curcumin inhibits HCV replication by induction of heme oxygenase-1 and suppression of AKT

Chen

Lee

Chuang

et al. 2012

International Journal of Molecular Medicine

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Although hepatitis C virus (HCV) affects approximately 130–170 million people worldwide, no vaccines are available. HCV is an important cause of chronic hepatitis, cirrhosis and hepatocellular carcinoma, leading to the need for liver transplantation. In this study, curcumin, a constituent used in traditional Chinese medicine, has been evaluated for its anti-HCV activity and mechanism, using a human hepatoma cell line containing the HCV genotype 1b subgenomic replicon. Below the concentration of 20% cytotoxicity, curcumin dose-dependently inhibited HCV replication by luciferase reporter gene assay, HCV RNA detection and HCV protein analysis. Under the same conditions, curcumin also dose-dependently induced heme oxygenase-1 with the highest induction at 24 h. Hemin, a heme oxygenase-1 inducer, also inhibited HCV protein expression in a dose-dependent manner. The knockdown of heme oxygenase-1 partially reversed the curcumin-inhibited HCV protein expression. In addition to the heme oxygenase-1 induction, signaling molecule activities of AKT, extracellular signal-regulated kinases (ERK) and nuclear factor-κB (NF-κB) were inhibited by curcumin. Using specific inhibitors of PI3K-AKT, MEK-ERK and NF-κB, the results suggested that only PI3K-AKT inhibition is positively involved in curcumin-inhibited HCV replication. Inhibition of ERK and NF-κB was likely to promote HCV protein expression. In summary, curcumin inhibited HCV replication by heme oxygenase-1 induction and AKT pathway inhibition. Although curcumin also inhibits ERK and NF-κB activities, it slightly increased the HCV protein expression. This result may provide information when curcumin is used as an adjuvant in anti-HCV therapy.

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Section: Introductionmentioning

confidence: 99%

Curcumin inhibits HCV replication by induction of heme oxygenase-1 and suppression of AKT

Chen

Lee

Chuang

et al. 2012

International Journal of Molecular Medicine

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“…All cell lines were grown at 37 °C under a 5% CO2 atmosphere. HEK293T cells were transfected by using CaHPO 4 method as previously described [18,19]. Transfection efficiency was evaluated by GFP visualization 24 h after transfection.…”

Section: Methodsmentioning

confidence: 99%

The metabolic regulator PGC‐1α links anti‐cancer cytotoxic chemotherapy to reactivation of hepatitis B virus

Rechtman

Burdelova

Bar-Yishay

et al. 2012

Journal of Viral Hepatitis

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Patients with chronic hepatitis B virus (HBV) infection are at an increased risk for a severe and a potentially fatal viral reactivation following anti-cancer therapy. The molecular mechanism for this induction of HBV expression is still unclear. Here, we show that treating hepatoma cell line expressing HBV with various anti-cancer cytotoxic agents results in a significant up-regulation of HBV expression. This HBV induction is at the transcriptional level and is time dependent. Interestingly, treating hepatoma cells with anti-cancer cytotoxic agents results in a robust induction of peroxisome proliferator-activated receptor-gamma coactivator-1α (PGC-1α), a metabolic and energy regulator that is normally induced in the liver under starvation conditions and that has been previously shown to strongly coactivate HBV transcription. Most importantly, HBV up-regulation following anti-cancer therapy depends on PGC-1α induction, because PGC-1α knock-down abolishes HBV induction. Finally, pretreatment of HBV-expressing cells with the antioxidant agent N-acetylcysteine attenuates the induction of both PGC-1α and HBV in response to anti-cancer treatment, suggesting that chemotherapy-associated PGC-1α induction is mediated by cellular oxidative stress that ultimately leads to HBV up-regulation. We conclude that cytotoxic anti-cancer chemotherapy has a direct and an immune system-independent effect on HBV gene expression, which is mediated by PGC-1α. Our results attribute to this metabolic regulator an unexpected role in linking anti-cancer treatment to HBV reactivation and make PGC-1α a potential target for future anti-HBV therapy, especially under conditions in which it is robustly induced, such as following anti-cancer treatment.

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“…Nevertheless, some promising observations have been made in cell culture and mouse model experiments. Several HDAC inhibitors have been shown to decrease cell proliferation , increase apoptosis , and to decrease both lipogenesis and gluconeogenesis . These effects could be beneficial for anti‐HCC treatment in HBV‐positive patients.…”

Section: Future Hepatitis B Treatment Optionsmentioning

confidence: 99%

Virus–host interplay in hepatitis B virus infection and epigenetic treatment strategies

et al. 2017

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Worldwide, chronic hepatitis B virus (HBV) infection is a major health problem and no cure exists. Importantly, hepatocyte intrusion by HBV particles results in a complex deregulation of both viral and host cellular genetic and epigenetic processes. Among the attempts to develop novel therapeutic approaches against HBV infection, several options targeting the epigenomic regulation of HBV replication are gaining attention. These include the experimental treatment with 'epidrugs'. Moreover, as a targeted approach, the principle of 'epigenetic editing' recently is being exploited to control viral replication. Silencing of HBV by specific rewriting of epigenetic marks might diminish viral replication, viremia, and infectivity, eventually controlling the disease and its complications. Additionally, epigenetic editing can be used as an experimental tool to increase our limited understanding regarding the role of epigenetic modifications in viral infections. Aiming for permanent epigenetic reprogramming of the viral genome without unspecific side effects, this breakthrough may pave the roads for an ambitious technological pursuit: to start designing a curative approach utilizing manipulative molecular therapies for viral infections in vivo.

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Erratum to “Curcumin inhibits hepatitis B virus via down‐regulation of the metabolic coactivator PGC‐1α” [FEBS Lett. 584 (2010) 2485–2490]

Cited by 18 publications

References 0 publications

Curcumin inhibits HCV replication by induction of heme oxygenase-1 and suppression of AKT

Curcumin inhibits HCV replication by induction of heme oxygenase-1 and suppression of AKT

The metabolic regulator PGC‐1α links anti‐cancer cytotoxic chemotherapy to reactivation of hepatitis B virus

Virus–host interplay in hepatitis B virus infection and epigenetic treatment strategies

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