Beyond viral dependence: The pathological consequences of HCV-induced EGF signaling

Suarez, Armando Andres Roca; Baumert, Thomas F.; Lupberger, Joachim

doi:10.1016/j.jhep.2018.05.033

Cited by 6 publications

(5 citation statements)

References 24 publications

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“…Moreover, among the pathways that we have identified to be epigenetically altered, the top pathway was cytoskeleton remodeling, which is known to be induced by EGFR signaling [7]. Other evidence supporting this hypothesis showed the association of the EGFR pathway with cirrhosis, fibrosis, and HCC, and the reversion of the expression of cirrhosis signature genes by the EGFR inhibitor erlotinib [62,63,[77][78][79]. Indeed, treatment with erlotinib reverted the expression and altered H3K9Ac levels for most of the signature genes in HCV-cured cells treated with DAAs.…”

Section: Possible Mechanisms Of Epigenetic Imprinting By Hcv Infection: Paving the Way For Hcc Prevention?mentioning

confidence: 62%

Tracking Down the Epigenetic Footprint of HCV-Induced Hepatocarcinogenesis

Domovitz

Gal-Tanamy

2021

JCM

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Hepatitis C virus (HCV) is a major cause of death and morbidity globally and is a leading cause of hepatocellular carcinoma (HCC). Incidence of HCV infections, as well as HCV-related liver diseases, are increasing. Although now, with new direct acting antivirals (DAAs) therapy available, HCV is a curable cancer-associated infectious agent, HCC prevalence is expected to continue to rise because HCC risk still persists after HCV cure. Understanding the factors that lead from HCV infection to HCC pre- and post-cure may open-up opportunities to novel strategies for HCC prevention. Herein, we provide an overview of the reported evidence for the induction of alterations in the transcriptome of host cells via epigenetic dysregulation by HCV infection and describe recent reports linking the residual risk for HCC post-cure with a persistent HCV-induced epigenetic signature. Specifically, we discuss the contribution of the epigenetic changes identified following HCV infection to HCC risk pre- and post-cure, the molecular pathways that are epigenetically altered, the downstream effects on expression of cancer-related genes, the identification of targets to prevent or revert this cancer-inducing epigenetic signature, and the potential contribution of these studies to early prognosis and prevention of HCC as an approach for reducing HCC-related mortality.

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Section: Possible Mechanisms Of Epigenetic Imprinting By Hcv Infection: Paving the Way For Hcc Prevention?mentioning

confidence: 62%

Tracking Down the Epigenetic Footprint of HCV-Induced Hepatocarcinogenesis

Domovitz

Gal-Tanamy

2021

JCM

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“…In the context of HCV infection, one of the best characterized signaling components associated with the development and progression of liver disease is the epidermal growth factor receptor (EGFR) pathway [51]. EGFR is an essential host factor regulating entry of the virus into hepatocytes [52] and is chronically deregulated in the liver of HCV-infected patients [52,53].…”

Section: Egf Signaling Pathwaymentioning

confidence: 99%

Hepatitis C Virus and Hepatocellular Carcinoma: When the Host Loses Its Grip

Goto

Suarez

Wrensch

et al. 2020

IJMS

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Chronic infection with hepatitis C virus (HCV) is a major cause of hepatocellular carcinoma (HCC). Novel treatments with direct-acting antivirals achieve high rates of sustained virologic response; however, the HCC risk remains elevated in cured patients, especially those with advanced liver disease. Long-term HCV infection causes a persistent and accumulating damage of the liver due to a combination of direct and indirect pro-oncogenic mechanisms. This review describes the processes involved in virus-induced disease progression by viral proteins, derailed signaling, immunity, and persistent epigenetic deregulation, which may be instrumental to develop urgently needed prognostic biomarkers and as targets for novel chemopreventive therapies.

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“…NO works as an inducer of apoptosis in some cell types and as an inhibitor of apoptosis in others, including hepatocytes [28]. Additionally, it was discovered that patients with HCV have increased inducible nitric oxide synthase (iNOS) expression, signaling excessive NO production that correlates favorably with viral load with hepatic inflammation [29]. The most conspicuous characteristic of HCV is its strong proclivity towards chronicity [30].…”

Section: ‫ـــــــــــــــــــــــــــــــــــــــــــــــــــــــــــ...mentioning

confidence: 99%

Measurement of the effect of 5-Fluorouracil as an anticancer drug on the nitric oxide levels on HepG2 cell line

Alnakib

Abdel-Hamid

Senduny

et al. 2022

Alfarama Journal of Basic & Applied Sciences

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Background: Carcinoma of the liver is the sixth most frequent malignancy in humans and is accountable for more than 600,000 deaths annually. According to the statistics, hepatocellular carcinoma patients typically die within a year after being diagnosed. As 5-fluorouracil (5-FU), the primary chemotherapeutic agent for most different types of cancers, is now routinely monitored via therapeutic drug monitoring, it has contributed to better clinical results. Many studies indicated the role of nitric oxide (NO) in different cancers as a pro-neoplastic or anti-neoplastic effector, but its function remains unclear in hepatocellular carcinoma (HCC). Aim of the study: The study's overall purpose was to look into the efficacy and toxicities of 5-fluorouracil on the biological behavior of HepG2 cell line by the methyl thiazole tetrazolium (MTT) assay and evaluate nitric oxide levels in monitoring the progression of HCC. Material and Methods: HepG2 cell line was incubated with different concentrations of 5-Fluorouracil as a chemotherapy drug. The effects of 5-Fluorouracil on cell proliferation, morphology, and the half-maximal inhibitory concentration (IC50) values were determined by the methyl thiazole tetrazolium (MTT). Results: The IC50 values for 5-Fluorouracil in HepG2 cells was (12.92±0.085μg), moreover the NO levels in the HepG2 cell line treated with 5-Fluorouracil were measured. We found significant inhibition in NO levels after treating HepG 2 cell lines by 5-Fluorouracil. Conclusion: The change in NO levels following chemotherapy helps predict treatment response in HepG-2 cells.

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Beyond viral dependence: The pathological consequences of HCV-induced EGF signaling

Abstract: W81XWH-16-1-0363). JL and AARS acknowledge the French Agence Nationale de Recherche sur le Sida et les Hépatites Virales (ANRS) (ECTZ4236; ECTZ4446). All authors thank Atish Mukherji (Inserm U1110, Strasbourg, France) for critical reading of the manuscript.

Cited by 6 publications

References 24 publications

Tracking Down the Epigenetic Footprint of HCV-Induced Hepatocarcinogenesis

Tracking Down the Epigenetic Footprint of HCV-Induced Hepatocarcinogenesis

Hepatitis C Virus and Hepatocellular Carcinoma: When the Host Loses Its Grip

Measurement of the effect of 5-Fluorouracil as an anticancer drug on the nitric oxide levels on HepG2 cell line

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