Association of Sat-a and Alu methylation status with HCV-induced chronic liver disease and hepatocellular carcinoma

Theodor Bilharz Research Institute

Bibliographic Information

Authors: El-Ahwany E.; Hassan M.; Elzallat M.; Abdelsalam L.; El-Sawy M.A.-H.; Seyam M.

Journal: Virus Research

Publisher: Elsevier B.V.

Publication Date: November 2022

Volume / Issue: Volume 321

Article No.: 198928

ISSN: 1681702

DOI: 10.1016/j.virusres.2022.198928

Scopus: View on Scopus

PubMed: 36100006

Document Type: Article

Authors and Affiliations

El-Ahwany E., Immunology Department, Theodor Bilharz Research Institute, Giza, Egypt; Hassan M., Immunology Department, Theodor Bilharz Research Institute, Giza, Egypt; Elzallat M., Immunology Department, Theodor Bilharz Research Institute, Giza, Egypt; Abdelsalam L., Human Genetics Department, Faculty of Medicine, Cairo University, Cairo, Egypt, Human Genetics Department, Faculty of Medicine, University of North Carolina, United States; El-Sawy M.A.-H., Hepato-Gastroenterology Department, Theodor Bilharz Research Institute, Giza, Egypt; Seyam M., Hepato-Gastroenterology Department, Theodor Bilharz Research Institute, Giza, Egypt

Abstract

Background: The combination of epigenetic and genetic abnormalities contributes together to the development of liver cancer. The methylation status of the repetitive elements (REs) in DNA has been investigated in a variety of human illnesses. However, the methylation patterns of Sat-α and Alu REs in chronic liver disease (CLD) and hepatocellular carcinoma (HCC) caused by hepatitis C virus (HCV) have never been studied before. Methodology: In this study, 3 groups of participants including 50 patients having HCV-induced CLD, 50 patients having HCV-induced HCC, and 46 healthy subjects were subjected to measurement of Sat-α and Alu methylation using the quantitative MethyLight assay. Results: Sat-α and Alu methylation percentages decreased significantly in both CLD and HCC, compared to control. Also, a significant Sat-α hypomethylation was detected in HCC, compared to CLD. In addition, Sat-α and Alu methylation showed a significant decline as lesion size grew. However, only Sat-α hypomethylation was significantly increased in association with portal vein thrombosis and the MELD score. Sat-α methylation percentage had the highest sensitivity and specificity for diagnosing HCC (100% and 84.4%) followed by α-fetoprotein (80% and 84.4%) and Alu methylation (66% and 61.5%). Furthermore, there was a strong positive correlation between Sat-α and Alu methylation. Conclusions: Measuring Sat-α and Alu methylation provides us with a new tool for early detecting HCV-induced CLD and hepatocarcinogenesis. Sat-α has the potential to be utilized as an independent predictive parameter for HCC development and progression because of its ability to distinguish between CLD and HCC with their different MELD scores. © 2022

Keywords

Alu; Chronic liver disease; DNA methylation; Hepatitis C virus; Hepatocellular carcinoma; Sat-α; alpha-Fetoproteins; Carcinoma, Hepatocellular; DNA; Hepacivirus; Hepatitis C; Humans; Liver Neoplasms; alanine aminotransferase; albumin; alpha fetoprotein; aspartate aminotransferase; bilirubin; adult; age; aged; alpha satellite repetitive elements; Alu repeat; Article; biochemical analysis; cancer staging; Child Pugh score; clinical article; correlational study; demographics; DNA structure; female; gender; human; international normalized ratio; liver cell carcinoma; male; Model For End Stage Liver Disease Score; platelet count; portal vein thrombosis; radiological parameters; sensitivity and specificity; virus pathogenesis; genetics; liver tumor

Citation Information

Scopus Citations: 2

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