Abstract
Like many human cancers, global DNA hypomethylation and promoter CpG island hypermethylation in tumor suppressor or tumor-related genes are frequently observed in gastric cancer, and aberrant DNA methylation occurs in a gene-specific manner during the multistep gastric carcinogenesis. Chronic Helicobacter pylori (H. pylori) infection induces pro-inflammatory cytokines and reactive oxygen and nitrogen species in the gastric mucosa, which is known to be associated with the accumulation of aberrant DNA methylation. Aberrant DNA methylation caused by H. pylori-associated gastritis persists even after the disappearance of H. pylori, and epigenetic alterations induced by H. pylori correlate with the risk for gastric cancer. Numerous microRNAs (miRNAs) are dysregulated during the gastric carcinogenesis, and some of these miRNAs are known to be also dysregulated by H. pylori infection. miRNAs dysregulated by H. pylori infection play an important role in gastric carcinogenesis by modulating inflammation and immune response of the host, cell cycle progression, apoptosis and proliferation, and tumor invasion and metastasis.
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