Journal
JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY
Volume 35, Issue 8, Pages 1347-1354Publisher
WILEY
DOI: 10.1111/jgh.15021
Keywords
DNA methylation; gastric cancer; gene-environment interaction; peripheral blood
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Background and Aim DNA methylation is an important epigenetic modification that can promote the development of various cancers. TheSTAT1andSOCS3have been observed to be hypermethylated in tumor tissues and peripheral blood. This study aimed to explore the relationship between the methylation status of theSTAT1andSOCS3in peripheral blood and gastric cancer (GC). Methods This hospital-based case-control study involved 372 patients with GC and 379 controls. The methylation status of theSTAT1andSOCS3was semiquantitatively determined using the methylation-sensitive high-resolution melting method. Logistic regression analysis was used to analyze the relationship between theSTAT1andSOCS3methylation status and GC susceptibility. Moreover, propensity scores were used to control confounding factors. Results Compared with negative methylation, the positive methylation ofSOCS3significantly increased the risk of GC (ORa = 1.820, 95% CI: 1.247-2.658,P = 0.002). This trend was also found via stratified analysis, and methylation positivity of theSOCS3significantly increased the risk of GC in the < 60 years group, in the >= 60 years group, and in the positiveHelicobacter pyloriinfection group (ORa = 1.654, 95% CI: 1.029-2.660,P = 0.038; ORa = 1.957, 95% CI: 1.136-3.376,P = 0.016; ORa = 2.084, 95% CI: 1.270-3.422,P = 0.004, respectively). Additionally, no significant association was found betweenSTAT1methylation and GC risk (ORa = 0.646, 95% CI: 0.363-1.147,P = 0.135). This study found that the interaction between the methylation status ofSTAT1andSOCS3and environmental factors did not have an impact on GC risk. Conclusion SOCS3methylation may serve as a new potential biomarker for GC susceptibility.
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