Integrin expression in
cancer tissues demonstrates its possible contribution to
tumor progression, invasion, and
metastasis. Helicobacter pylori (H. pylori)
infection is related to
gastric cancer and gastric
inflammation. H. pylori induced upregulation in expression of
integrin in gastric epithelia cells.
Reactive oxygen species (ROS) are considered as an important regulator in the pathogenesis of H. pylori-induced gastric ulceration and
carcinogenesis.
Integrin expression may be regulated by
oxidant-sensitive
transcription factors,
nuclear factor-kappaB (
NF-kappaB) and
activator protein-1 (AP-1). The present study aims to investigate whether H. pylori in a Korean isolate (HP99) induces the expression of
integrin alpha5 and
integrin beta1, and whether H. pylori-induced expression of
integrin alpha5 and
integrin beta1 are inhibited in the cells transfected with mutant genes for Ras (ras N-17), c-Jun (TAM-67), and IkappaBalpha(MAD-3) or treated with DPI, an inhibitor of
NADPH oxidase. As a result, H. pylori induced the expression of
integrin alpha5 and
integrin beta1 in gastric
adenocarcinoma (AGS) cells time-dependently. Treatment of DPI or transfection with mutant genes for Ras (ras N-17), c-jun (TAM67), and
IkappaBalpha(MAD3) inhibited H. pylori-induced expression of
integrin alpha5 and
integrin beta1 in AGS cells. In conclusion, H. pylori activates Ras,
NF-kappaB, and
AP-1 and thus induces the expression of
integrin alpha5 and
integrin beta1 in gastric epithelial cells. Inhibition of ROS production by DPI suppressed the expression of
integrin alpha5 and
integrin beta1 in gastric epithelial cells. The results suggest the possible involvement of
NADPH oxidase for ROS production in H. pylori-infected gastric epithelial cells.