Gene methylation is an epigenetic alteration in hepatocellular carcinoma (HCC), and hepatitis B virus (HBV) plays a crucial role in carcinogenesis of HCC. However, the association between gene methylation and HBV infection in HCC remains unclear. In our study, we conducted a comprehensive meta-analysis to evaluate the association. A total of 1,148 studies were initially retrieved from some literature database. After a four-step filtration, we obtained 69 case-control studies in this meta-analysis. Our results showed six genes (, , , , and ) in HBV-positive carcinoma tissues, one gene () in HBV-positive adjacent tissues and two gene ( and ) in HBV-positive carcinoma serums, which were significantly hypermethylated. Subgroup meta-analysis by geographical populations revealed that methylation was significantly higher in HBV-positive carcinoma tissues in China and Japan. In addition, and methylation was significantly higher in China but not in Japan. Our study indicated that HBV infection could induce DNA methylation in HCC and DNA methylation could lead to the development of HBV-related HCC.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6856736PMC
http://dx.doi.org/10.7150/jca.33005DOI Listing

Publication Analysis

Top Keywords

gene methylation
12
hbv infection
12
hbv-positive carcinoma
12
association gene
8
methylation hbv
8
hepatocellular carcinoma
8
carcinoma tissues
8
tissues gene
8
gene hbv-positive
8
methylation higher
8

Similar Publications

Objective: Myocardial ischemia-reperfusion injury (MIRI) is a highly complex disease with high morbidity and mortality. Studying the molecular mechanism of MIRI and discovering new targets are crucial for the future treatment of MIRI.

Methods: We constructed the MIRI rat model and hypoxia/reoxygenation (H/R) injury cardiomyocytes model.

View Article and Find Full Text PDF

Non-small cell lung cancer (NSCLC) has emerged as one of the most prevalent malignancies worldwide. N6-methyladenosine (mA) methylation, a pervasive epigenetic modification in long noncoding RNAs (lncRNAs), plays a crucial role in NSCLC progression. Here, we report that mA modification and the expression of the lncRNA stem cell inhibitory RNA transcript (SCIRT) was significantly upregulated in NSCLC tissues and cells.

View Article and Find Full Text PDF

Flowering, a pivotal plant lifecycle event, is intricately regulated by environmental and endogenous signals via genetic and epigenetic mechanisms. Photoperiod is a crucial environmental cue that induces flowering by activating integrators through genetic and epigenetic pathways. However, the specific role of DNA methylation, a conserved epigenetic marker, in photoperiodic flowering remains unclear.

View Article and Find Full Text PDF

A Recursive Model Approach to Include Epigenetic Effects in Genetic Evaluations Using Simulated DNA Methylation Effects.

J Anim Breed Genet

January 2025

Departamento de Mejora Genética Animal, Instituto Nacional de Investigación y Tecnología Agraria y Alimentaria (INIA), CSIC, Madrid, Spain.

The advancement of epigenetics has highlighted DNA methylation as an intermediate-omic influencing gene regulation and phenotypic expression. With emerging technologies enabling the large-scale and affordable capture of methylation data, there is growing interest in integrating this information into genetic evaluation models for animal breeding. This study used methylome information from six dairy cows to simulate the methylation profile of 13,183 genotyped animals.

View Article and Find Full Text PDF

Hepatocellular carcinoma (HCC) is the most common primary liver cancer. Hepatitis B virus (HBV) is the main pathogen for HCC development. HBV covalently closed circular DNA (cccDNA) forms extra-host chromatin-like minichromosomes in the nucleus of hepatocytes with host histones, non-histones, HBV X protein (HBx) and HBV core protein (HBc).

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!