Fig. 5

H. pylori regulates the GNB4 expression and demethylation modification through induction of TET1 expression. A GEPIA analysis revealed that GNB4 expression was significantly correlated with TET1 in patients with GC (Spearman method, R = 0.51, P < 0.001). B qRT-PCR analysis of TET1, TET2, and TET3 mRNA expression in GES1 and MKN45 cells uninfected or infected with H. pylori strains (26695 and SS1; 6 h). C The expression of CagA, TET1, DNMT1, and GNB4 proteins in GES1 and MKN45 cells uninfected or infected with H. pylori strains (26695 and SS1; 6 h) was determined through western blotting. D Western blot analysis of TET1 expression in MKN45 cells treated with TET1 siRNA. E Promoter methylation level of GNB4 in MKN45 cells treated TET1 siRNA through MSP. F Western blot analysis of TET1 and GNB4 expression in MKN45 cells following treatment with different concentrations of doxycycline (DOX) for 24 h. G Schematic description of the experimental design for establishing the animal model. H qRT-PCR analysis of GNB4 and TET1 expression in the gastric mucosa of different groups of mice. I Pattern diagram showing the two primer amplification regions designed in the differentially methylated region (DMR, − 331 to − 11 bp) of GNB4 promoter in ChIP-qPCR. J ChIP-PCR analysis of the GNB4 expression in MKN45 cells transfected with NC and TET1 siRNA to examine the binding of TET1 and the DMR of GNB4 promoter. K Five enriched diseases and regulated genes according to differential GNB4 expression in the TCGA database (using Metascape online tool). L Western blot analysis of CagA, p-NF-κB(S536), and NF-κB protein expression in AGS and MKN45 cells uninfected or infected with H. pylori strains (26695 and SS1; 6 h). M Western blot analysis of TET1, p-NF-κB(S536), NF-κB, and GNB4 protein expression in AGS and MKN45 cells treated with PDTC (NF-κB inhibitor; 10 and 20 μM for AGS and MKN45 cells, respectively) for 12 h