Abstract
DNA methylation is an epigenetic mechanism used by cells to control gene expression. DNA methylation is a commonly used epigenetic signaling tool that can hold genes in the “off” position. Chronic infection with hepatitis C virus (HCV) is considered a major risk for chronic liver impairment. It is the most common leading cause of HCC. The present work is aimed at studying whole genome 5′-methylcytosine levels in cirrhotic HCV-infected Egyptian patients. In the present study, 120 Egyptian adults were included. They were divided into two groups: group І (40 apparently healthy control subjects) and group ІІ (80 HCV-infected patients). Furthermore, group II was subdivided into 2 subgroups according to the presence of HCC in HCV-infected subjects. To all studied subjects, the level of 5-mC% was measured in peripheral blood. In the present study, the median of 5′-methylcytosine% in the control group (group I) was 2.5, in the HCV group (group IIa) was 2.45, and in the HCC group (group II b) was 2.25. A stepwise decrease in 5′-methylcytosine% from the control (group I) toward HCC (group IIb) was observed, taking into consideration that the stepwise global hypomethylation was not statistically significant (p = 0.811). There was a negative correlation between ALT and 5′-methylcytosine% (p = −0.029). From this study, we can conclude that global DNA 5′-methylcytosine% does not differ in HCV-infected cirrhotic patients and HCC patients when compared to normal controls. Consecutively, we had concluded that there is no impact of 5′-methylcytosine% on the development of liver cirrhosis or HCC. Moreover, the negative correlation between 5′-methylcytosine% and serum ALT level denotes a trend of decrease in 5′-methylcytosine% with more liver damage.
Highlights
Epigenetics refers to heritable changes in gene expression without changes to the underlying DNA sequence
Reactive oxygen species (ROS) induced by chronic hepatitis C virus (HCV) infection could change histone modification to the repressive form at CpG islandcontaining tumor suppressor gene promoters, leading to tumor suppressor gene inactivation. These findings suggest that chronic inflammation associated with HCV infection might cause epigenetic alterations by the immune response as well as through the induction of oxidative stress [17, 18, 19]
To all the studied subjects, the following was done: (i) Detailed history taken from all subjects including history of bleeding, encephalopathy, jaundice, and ascites (ii) Complete physical examination done to all subjects (iii) X-ray chest (iv) Abdominal ultrasound [21]: diagnosis of liver cirrhosis was based on clinical manifestations, biochemical markers, and ultrasonographic features of liver cirrhosis
Summary
Epigenetics refers to heritable changes in gene expression without changes to the underlying DNA sequence. Disordered epigenetic gene regulation is a feature of a number of important human diseases as neurodevelopmental disorders, cardiovascular disease, and cancer [3, 4]. A number of processes have been implicated in epigenetic gene regulation including DNA methylation, chromatin structure remodeling, histone modification, and noncoding RNAs [5]. DNA methylation refers to the addition of a methyl group (CH3) covalently to the base cytosine (C) in the dinucleotide 5′-CpG-3′ [6]. Genome-wide high-resolution DNA methylablast cell line demonstrated that 67.7% of CpGs are methylated [7]. The addition of methyl groups is controlled at several different levels in cells and is carried out by a family of enzymes called DNA methyltransferases (DNMTs) [8]. DNA methylation patterns are a product of the frequency of cytosine DNA methylation at specific sites along a strand
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