BACKGROUND AND AIM: H. pylori interacts with gastric epithelial cells, which may activate signaling pathways important for gastric cancer invasion. Ezrin, a membrane cytoskeletal crosslinker protein, is well documented to regulate cell adhesion and cell motility. The aim of the present study was to determine whether ezrin is involved in H. pylori-induced cancer cell motility and invasion. METHODS: The VIL-2 of RNA interference plasmid vector and control plasmid vector were constructed. AGS (a human gastric adenocarcinoma cell line) cells were transfected by these plasmid vectors. The stable expression cell lines AGS(ezrin) was obtained by G418 resistance screening. The express levels of ezrin protein and the cellular invasive potential of four groups, including the AGS control, AGS(ezrin) control, AGS co-culture with H. pylori, AGS(ezrin) co-culture with H. pylori were detected. Meanwhile, the morphology, cell migration and adhesion were determined respectively. RESULTS: Co-culture with H. pylori stimulated AGS cell motility and invasion, up-regulated ezrin expression at the protein level and induced a Hummingbird phenotype. The silencing of ezrin expression suppressed the motility and invasion of gastric cancer cells and inversed the cell invasion phenotype and enhanced the ability for cell adhesion. CONCLUSION: Knockdown of ezrin by RNAi suppresses H. pylori-enhanced migration and invasion of gastric cancer cells. These findings indicate that ezrin may play a key role in the migration and invasion of gastric cancer cells, and thus may be a therapeutic target to prevent metastasis of gastric cancer promoted by H. pylori infection.
BACKGROUND AND AIM: H. pylori interacts with gastric epithelial cells, which may activate signaling pathways important for gastric cancer invasion. Ezrin, a membrane cytoskeletal crosslinker protein, is well documented to regulate cell adhesion and cell motility. The aim of the present study was to determine whether ezrin is involved in H. pylori-induced cancer cell motility and invasion. METHODS: The VIL-2 of RNA interference plasmid vector and control plasmid vector were constructed. AGS (a humangastric adenocarcinoma cell line) cells were transfected by these plasmid vectors. The stable expression cell lines AGS(ezrin) was obtained by G418 resistance screening. The express levels of ezrin protein and the cellular invasive potential of four groups, including the AGS control, AGS(ezrin) control, AGS co-culture with H. pylori, AGS(ezrin) co-culture with H. pylori were detected. Meanwhile, the morphology, cell migration and adhesion were determined respectively. RESULTS: Co-culture with H. pylori stimulated AGS cell motility and invasion, up-regulated ezrin expression at the protein level and induced a Hummingbird phenotype. The silencing of ezrin expression suppressed the motility and invasion of gastric cancer cells and inversed the cell invasion phenotype and enhanced the ability for cell adhesion. CONCLUSION: Knockdown of ezrin by RNAi suppresses H. pylori-enhanced migration and invasion of gastric cancer cells. These findings indicate that ezrin may play a key role in the migration and invasion of gastric cancer cells, and thus may be a therapeutic target to prevent metastasis of gastric cancer promoted by H. pyloriinfection.