BACKGROUND: DNA methylation is an important epigenetic modification that can promote the development of various cancers. The STAT1 and SOCS3 have been observed to be hypermethylated in tumor tissues and peripheral blood. This study aimed to explore the relationship between the methylation status of the STAT1 and SOCS3 in 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 the STAT1 and SOCS3 was semi-quantitatively determined using the methylation-sensitive high-resolution melting method. Logistic regression analysis was used to analyze the relationship between the STAT1 and SOCS3 methylation status and GC susceptibility. Moreover, propensity scores were used to control confounding factors. RESULTS: Compared with negative methylation, the positive methylation of SOCS3 significantly 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 the SOCS3 significantly increased the risk of GC in the <60 years group, in the ≥60 years group and in the positive Helicobacter pylori infection 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 between STAT1 methylation 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 of STAT1 and SOCS3 and environmental factors did not have an impact on GC risk. CONCLUSION: SOCS3 methylation may serve as a new potential biomarker for GC susceptibility. This article is protected by copyright. All rights reserved.
BACKGROUND: DNA methylation is an important epigenetic modification that can promote the development of various cancers. The STAT1 and SOCS3 have been observed to be hypermethylated in tumor tissues and peripheral blood. This study aimed to explore the relationship between the methylation status of the STAT1 and SOCS3 in 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 the STAT1 and SOCS3 was semi-quantitatively determined using the methylation-sensitive high-resolution melting method. Logistic regression analysis was used to analyze the relationship between the STAT1 and SOCS3 methylation status and GC susceptibility. Moreover, propensity scores were used to control confounding factors. RESULTS: Compared with negative methylation, the positive methylation of SOCS3 significantly 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 the SOCS3 significantly increased the risk of GC in the <60 years group, in the ≥60 years group and in the positive Helicobacter 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 between STAT1 methylation 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 of STAT1 and SOCS3 and environmental factors did not have an impact on GC risk. CONCLUSION:SOCS3 methylation may serve as a new potential biomarker for GC susceptibility. This article is protected by copyright. All rights reserved.
Entities:
Keywords:
DNA methylation; gastric cancer; gene-environment interaction; peripheral blood