DNA Methylation-Mediated Overexpression of in -Induced Gastric Cancer: In Silico- and In Vitro-Based Identification of a Potential Biomarker for Carcinogenesis.

Given the high global prevalence and mortality associated with gastric cancer, and its known causal link with infection, it is important to have a biomarker to identify malignant transformation at early stages. Previously, we, and others, have reported that -induced epigenetic changes could mediate carcinogenic transformation of the gastric cells. Also, CXCL1 secreted by gastric cancer cells was reported as a key diagnostic and prognostic biomarker for the pathogenic progression of gastric cancer. In this study, for the first time, we aimed to investigate the role of -induced DNA methylation-based epigenetic regulation of . In silico analysis of publicly available datasets and in vitro experiments were performed. Our results showed that is highly expressed in both gastric cancer tissues and gastric cancer cells infected with . Further, we showed and confirmed that -mediated overexpression of is due to hypomethylation of its promoter region. Since epigenetic events such as DNA methylation happen early in the sequence; -induced hypomethylation could likely be detected at an early stage of gastric cancer development. Epigenetic modifications, such as hypomethylation, are reversible and could potentially be a therapeutic target using demethylation drugs.