Hepatitis B virus (HBV) infection led to 66% liver deaths world-wide in year 2015. Thirty-seven per cent of these deaths were the result of chronic hepatitis B (CHB)-associated hepatocellular carcinoma (HCC). Although early diagnosis of HCC improves survival, early detection is rare. Methylation of HBV DNA including covalently closed circular DNA (cccDNA) is more often encountered in HCC cases than those in CHB and cirrhosis. Three typical CpG islands within the HBV genome are the common sites for methylation. The HBV cccDNA methylation affects the viral replication and protein expression in the course of infection and may associate with the disease pathogenesis and HCC development. We review the current findings in HBV DNA methylation that provide insights into its role in HCC diagnosis.

The intestinal tract is the entry gate for nutrients and symbiotic organisms, being in constant contact with external environment. DNA methylation is one of the keys to how environmental conditions, diet and nutritional status included, shape functionality in the gut and systemically. This review aims to summarise findings on the importance of methylation to gut development, differentiation and function. Evidence to date on how external factors such as diet, dietary supplements, nutritional status and microbiota modifications modulate intestinal function through DNA methylation is also presented.

The aim of the present review paper is to survey the literature related to DNA methylation, and its association with cancer and ageing. The review will outline the key factors, including diet, which modulate DNA methylation. Our rationale for conducting this review is that ageing and diseases, including cancer, are often accompanied by aberrant DNA methylation, a key epigenetic process, which is crucial to the regulation of gene expression. Significantly, it has been observed that with age and certain disease states, DNA methylation status can become disrupted. For instance, a broad array of cancers are associated with promoter-specific hypermethylation and concomitant gene silencing. This review highlights that hypermethylation, and gene silencing, of the EN1 gene promoter, a crucial homeobox gene, has been detected in various forms of cancer. This has led to this region being proposed as a potential biomarker for diseases such as cancer. We conclude the review by describing a recently developed novel electrochemical method that can be used to quantify the level of methylation within the EN1 promoter and emphasise the growing trend in the use of electrochemical techniques for the detection of aberrant DNA methylation.

In order to probe the effect of methylation on heterosis, the methylation-sensitive arbitrarily primed polymerase chain reaction (AP-PCR) technique was adopted to amplify pig genome DNA with 40 single arbitrary primers. The material involved parental lines and F1 hybrids of Large White×Meishan crosses. Nineteen differentially methylated sites with RsaI+HpaII digestion and 14 differentially methylated sites with RsaI+MspII digestion between parental lines and the hybrid were found. All fragments detected in this study were grouped into four classes: (1) the same level of methylation in both parental lines and the hybrid; (2) the same level of methylation in one parent and the hybrid; (3) an increased level of methylation in the hybrid compared to the parents, and (4) a decreased level of methylation in the hybrid. Five sites had significant effects on seven traits (P<0.05). Sequence analysis showed that three sequences had a high-identity match in GenBank (greater than 87%) and two sequences had no match in the database. The percentage of G+C in three sequences was over 50, and the observed/expected CpG of all sequences was above 0.6. Furthermore, one sequence contained G/C boxes. This study demonstrated that the sites in CpG islands within a gene promoter were differentially methylated in the hybrid compared to parental lines; methylated sites contributed differentially to F1 performance, showing that heterosis could benefit from either expression or repression of some genes.