Epigenetic alterations due to diet and Helicobacter pylori infection in gastric carcinogenesis

Abstract

Sporadic gastric cancer is considered to be the result of a progressive accumulation of genotypic changes due to an adverse environment (i.e., diet and Helicobacter pylori infection). The main molecular mechanism implicated in cancer-related molecular alterations is of epigenetic nature, which includes DNA methylation and histone modification. Diet may influence the methylation status supplying methyl groups S-adenosyl-methionine formation, modifying DNA methyltransferase activity and influencing DNA demethylation activity. H. pylori may affect DNA methyltransferase directly or through inflammatory mediators (e.g., reactive oxygen species or nitric oxide). In conclusion, gastric cancer is a multistep process due to an adverse environment over a long period of time. Dietary habit and H. pylori infection can induce epigenetic alterations that, in turn, trigger gastric carcinogenesis.

Keywords::

• diet
• DNA methylation
• gastric carcinogenesis
• Helicobacter pylori infection
• histone acetylation

Financial & competing interests disclosure

The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.

No writing assistance was utilized in the production of this manuscript.