Taken together, LMP2A induced the phosphorylation of ERK, which activated DNMT3a transcription and caused AQP3 expression loss through CpG island methylation of AQP3 promoter in EBVaGC.
Our current studies identify the mechanistic link between H. pylori infection and AQP3 upregulation in the pathogenesis of gastric carcinoma, which involves the activation of the ROS-HIF-1α axis and the exacerbated ROS-HIF-1α-AQP3-ROS loop.
Accordingly, we analyzed the association between a single-nucleotide polymorphism locus of aquaporin 3 (rs2231231) and Epstein-Barr virus (EBV)-associated nasopharyngeal carcinoma (EBVaNPC), lymphoma (EBVaL), and gastric carcinoma in China.
However, the relationships of AQP3 with GIM classification and with other proteins, and their roles in the transition from GIM to gastric carcinoma (GC) remain unknown.
In this study, we observed that AQP3 expression was upregulated in tumor tissues, and positively correlated with tumor size, lymph node metastasis and glycerol concentration in human GC samples.
To investigate the characteristics of GIM in non-cancerous tissues adjacent to GC, as well as the expression and role of AQP3 in GIM tissues, 16 patients diagnosed with gastric adenocarcinoma of intestinal type located in the lesser curve of the antrum were consecutively enrolled in this study.
Our previous studies showed that aquaporin 3 (AQP3) is overexpressed in gastric carcinoma and promotes the migration and proliferation of human gastric carcinoma cells, suggesting that AQP3 may be a potentially important determinant of gastric carcinoma.