HCV and HCC Tango-Deciphering the Intricate Dance of Disease: A Review Article.
Ivana MilosevicNevena TodorovicAna FilipovicJelena SimicMarko MarkovicOlja StevanovicJovan MalinicNatasa KatanicNikola MitrovicNatasa NikolicPublished in: International journal of molecular sciences (2023)
Hepatitis C virus (HCV) is a major cause of hepatocellular carcinoma (HCC) accounting for around one-third of all HCC cases. Prolonged inflammation in chronic hepatitis C (CHC), maintained through a variety of pro- and anti-inflammatory mediators, is one of the aspects of carcinogenesis, followed by mitochondrial dysfunction and oxidative stress. Immune response dysfunction including the innate and adaptive immunity also plays a role in the development, as well as in the recurrence of HCC after treatment. Some of the tumor suppressor genes inhibited by the HCV proteins are p53, p73, and retinoblastoma 1. Mutations in the telomerase reverse transcriptase promoter and the oncogene catenin beta 1 are two more important carcinogenic signaling pathways in HCC associated with HCV. Furthermore, in HCV-related HCC, numerous tumor suppressor and seven oncogenic genes are dysregulated by epigenetic changes. Epigenetic regulation of gene expression is considered as a lasting "epigenetic memory", suggesting that HCV-induced changes persist and are associated with liver carcinogenesis even after cure. Epigenetic changes and immune response dysfunction are recognized targets for potential therapy of HCC.
Keyphrases
- hepatitis c virus
- gene expression
- immune response
- oxidative stress
- dna methylation
- human immunodeficiency virus
- anti inflammatory
- genome wide
- diabetic rats
- signaling pathway
- epithelial mesenchymal transition
- dendritic cells
- dna damage
- cell proliferation
- stem cells
- toll like receptor
- risk assessment
- inflammatory response
- liver fibrosis
- heat stress
- induced apoptosis
- drug induced
- bioinformatics analysis
- heat shock
- polycyclic aromatic hydrocarbons
- human health