Unraveling the Molecular Mechanisms Involved in HCV-Induced Carcinogenesis

Cancer induced by a viral infection is among the leading causes of cancer. Hepatitis C Virus (HCV) is a hepatotropic oncogenic positive-sense RNA virus that leads to chronic infection, exposing the liver to a continuous process of damage and regeneration and promoting hepatocarcinogenesis. The virus...

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Bibliographic Details
Published in:Viruses 2022-12, Vol.14 (12), p.2762
Main Authors: Heredia-Torres, Tania Guadalupe, Rincón-Sánchez, Ana Rosa, Lozano-Sepúlveda, Sonia Amelia, Galan-Huerta, Kame, Arellanos-Soto, Daniel, García-Hernández, Marisela, Garza-Juarez, Aurora de Jesús, Rivas-Estilla, Ana María
Format: Article
Language:English
Subjects:
Analysis
Antiviral agents
Antiviral Agents - pharmacology
Apoptosis
Carcinogenesis
Carcinogenesis - genetics
Carcinoma, Hepatocellular - genetics
Chromatin remodeling
Chronic infection
DNA methylation
Epigenesis, Genetic
Epigenetics
epithelial-mesenchymal transition
Genomic instability
Hepacivirus - genetics
Hepatitis C
Hepatitis C - drug therapy
Hepatitis C virus
Hepatitis C, Chronic - drug therapy
Hepatocellular carcinoma
Humans
inflammation
Kinases
Liver cancer
Liver Neoplasms - genetics
Mesenchyme
Molecular modelling
Oxidative stress
Prevention
proliferation
Review
RNA viruses
Steatosis
Therapeutic targets
Viral infections
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Summary:Cancer induced by a viral infection is among the leading causes of cancer. Hepatitis C Virus (HCV) is a hepatotropic oncogenic positive-sense RNA virus that leads to chronic infection, exposing the liver to a continuous process of damage and regeneration and promoting hepatocarcinogenesis. The virus promotes the development of carcinogenesis through indirect and direct molecular mechanisms such as chronic inflammation, oxidative stress, steatosis, genetic alterations, epithelial-mesenchymal transition, proliferation, and apoptosis, among others. Recently, direct-acting antivirals (DAAs) showed sustained virologic response in 95% of cases. Nevertheless, patients treated with DAAs have reported an unexpected increase in the early incidence of Hepatocellular carcinoma (HCC). Studies suggest that HCV induces epigenetic regulation through non-coding RNAs, DNA methylation, and chromatin remodeling, which modify gene expressions and induce genomic instability related to HCC development that persists with the infection's clearance. The need for a better understanding of the molecular mechanisms associated with the development of carcinogenesis is evident. The aim of this review was to unravel the molecular pathways involved in the development of carcinogenesis before, during, and after the viral infection's resolution, and how these pathways were regulated by the virus, to find control points that can be used as potential therapeutic targets.
ISSN:1999-4915
1999-4915
DOI:10.3390/v14122762