Effect of H. pylori on the expression of CCAAT enhancer binding protein α and Cx43 and its role in gastric carcinogenesis / 中南大学学报(医学版)

ABSTRACT

OBJECTIVE@#To explore the effect of H. pylori on the expression of CCAAT enhancer binding protein α (C/EBPα) and connexin 43 (Cx43) in gastric carcinogenesis.
@*METHODS@#Different gastric mucosal epithelial cell lines (GES-1 cells, AGS cells and SGC-7901 cells) were cultured. A total of 6 cases of chronic non-atrophic gastritis tissues, 12 cases of gastric precancerous lesions tissues and 12 cases of gastric cancer tissues were collected under endoscopy. The expression of C/EBPα and Cx43 mRNA in the above-mentioned cells and tissues was detected by real-time PCR. The GES-1 cells and East Asian CagA+ H. pylori strains were co-cultured for 24 and 48 h as an experimental group, and those cell lines without H. pylori infection were cultured for 24 and 48 h as a control group. Real-time PCR and Western bolt were used to detect the expression of mRNA and proteins of C/EBPα and Cx43 in GES-1 cells, respectively.
@*RESULTS@#The expressions of C/EBPα and Cx43 mRNA in the AGS and SGC-7901 cells were lower than those in GES-1 cells (all P<0.05), and both of them decreased more profoundly in the SGC-7901 cells than those in the AGS cells (both P<0.05). The expressions of C/EBPα and Cx43 mRNA were lower in the gastric cancer tissues than those in the chronic non-atrophic gastritis tissues (both P<0.05) and gastric precancerous lesion tissues (both P<0.05). The C/EBPα expression was positively correlated with Cx43 expression (gastric precancerous lesion tissues: r=0.679, gastric cancer tissues: r=0.792; both P<0.05). Compared with the control group, the expressions of C/EBPα and Cx43 mRNA and protein in the experimental group were decreased at 24 and 48 h after culture (both P<0.05), which were lower at 48 h than those at 24 h (both P<0.05).
@*CONCLUSION@#H. pylori infection can down-regulate the expressions of C/EBPα and Cx43 on gastric epithelial cells, which may be associated with gastric carcinogenesis.