TY - GEN
T1 - Signaling for integrin α5/β1 expression in Helicobacter pylori-infected gastric epithelial AGS cells
AU - Soon, Ok Cho
AU - Kyung, Hwan Kim
AU - Yoon, Joo Heon
AU - Kim, Hyeyoung
PY - 2006/12
Y1 - 2006/12
N2 - 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-κB (NF-κB) and activator protein-1 (AP-1). The present study aims to investigate whether H. pylori in aKorean isolate (HP99) induces the expression of integrin α5 and integrin β1, and whether H. pylori-induced expression of integrin α5 and integrin β1 are inhibited in the cells transfected with mutant genes for Ras (ras N-17), c-Jun (TAM-67), and IκBα(MAD-3) or treated with DPI, an inhibitor of NADPH oxidase. As a result, H. pylori induced the expression of integrin α5 and integrin β1 in gastric adenocarcinoma (AGS) cells time-dependently. Treatment of DPI or transfection with mutant genes for Ras (ras N-17), c-jun (TAM67), and IκBα(MAD3) inhibited H. pylori-induced expression of integrin α5 and integrin β1 in AGS cells. In conclusion, H. pylori activates Ras, NF-κB, and AP-1 and thus induces the expression of integrin α5 and integrin β1 in gastric epithelial cells. Inhibition of ROS production by DPI suppressed the expression of integrin α5 and integrin β1 in gastric epithelial cells. The results suggest the possible involvement of NADPH oxidase for ROS production in H. pylori-infected gastric epithelial cells.
AB - 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-κB (NF-κB) and activator protein-1 (AP-1). The present study aims to investigate whether H. pylori in aKorean isolate (HP99) induces the expression of integrin α5 and integrin β1, and whether H. pylori-induced expression of integrin α5 and integrin β1 are inhibited in the cells transfected with mutant genes for Ras (ras N-17), c-Jun (TAM-67), and IκBα(MAD-3) or treated with DPI, an inhibitor of NADPH oxidase. As a result, H. pylori induced the expression of integrin α5 and integrin β1 in gastric adenocarcinoma (AGS) cells time-dependently. Treatment of DPI or transfection with mutant genes for Ras (ras N-17), c-jun (TAM67), and IκBα(MAD3) inhibited H. pylori-induced expression of integrin α5 and integrin β1 in AGS cells. In conclusion, H. pylori activates Ras, NF-κB, and AP-1 and thus induces the expression of integrin α5 and integrin β1 in gastric epithelial cells. Inhibition of ROS production by DPI suppressed the expression of integrin α5 and integrin β1 in gastric epithelial cells. The results suggest the possible involvement of NADPH oxidase for ROS production in H. pylori-infected gastric epithelial cells.
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U2 - 10.1196/annals.1378.032
DO - 10.1196/annals.1378.032
M3 - Conference contribution
C2 - 17384273
AN - SCOPUS:34247608221
SN - 1573316458
SN - 9781573316453
T3 - Annals of the New York Academy of Sciences
SP - 298
EP - 304
BT - Signal Transduction Pathways, Part A
PB - Blackwell Publishing Inc.
ER -
