Helicobacter pylori cytotoxin associated protein CagA up-regulating gastrin gene expression

Abstract

Objective To study whether Helicobacter pylori CagA protein can control gastrin gene expression and the detailed mechanism. Methods First, pcDNA3. 1ZEO (-)/cagA7 was transfected into gastric cancer cell lines AGS and SGC-7901 cells. At the same time, culturing the Helicobacter pylori NCTC11637 and infecting AGS and SGC-7901 cells with it. Next, in the infected and transfecled AGS and SGC-7901 cells, respectively adding the JAK2 signaling pathway inhibitor AG490 and the ERK signaling pathway inhibitor U0126 to inhibit the two signaling pathway. Untreated gastric cancer cells and empty vector transfected cells as the control. Using real-time fluorescence quantitative PCR to detect the levels of gastrin mRNA in transfected and infected cells. Results After AGS and SGC-7901 cells were transfected with pcDNA3. lZE0(-)/cagA7 and infected with NCTC11637, the results showed that the expression of gastrin mRNA increased significantly (P ＜ 0. 05) in transfected and infected cells as compared with the control group, but after adding the inhibitor AG490 and U0126 respectively, the expression of gastrin mRNA decreased significantly(P＜0.05). Conclution These results suggest that CagA may up-regulate the expression of the gastrin gene, and CagA is one of the important proteins in regulating gastrin gene expression. The ERK/MAPK and JAK/STAT signaling pathways may be involved in controlling of gastrin gene expression by CagA. Key words: Helicobacter pylon; Gastrin; CagA; ERK/MAPK; JAK/STAT