title: Cell adhesion-related gene expression by Helicobacter pylori in gastric epithelial AGS cells.
abstract: Helicobacter pylori (H. pylori) infection leads to gastroduodenal inflammation, peptic ulceration and gastric carcinoma. H. pylori may induce disease-specific gene expression in gastric epithelial cells. cDNA microarray for 352 cancer-related genes was used to identify the genes altered by H. pylori (cagA positive) in gastric epithelial AGS cells. Expressions of the genes identified on the microarray and other genes closely associated with these genes were determined by reverse transcriptase-polymerase chain reaction (RT-PCR). Western blot analysis and cell adhesion assay were performed to confirm the protein levels of the genes and the role of the genes on cell adhesion in H. pylori-infected AGS cells. As a result, the expression of four genes (galectin 1, aldolase A, integrin alpha5, LIM domain only 7 (LMO7)) were up-regulated by H. pylori in AGS cells, determined by cDNA microarray. RT-PCR analysis showed that the genes up-regulated by H. pylori were the genes regulating cell-cell adhesion and cell-extracellular matrix interaction, such as galectin-1 and galectin-3, integrin alpha5, and LIM domain only 7 (LMO7), and cancer-related glycolytic enzyme aldolase A and C. Cell adhesion to extracellular matrix proteins such as poly-L-lysine and fibronectin was mediated by H. pylori-induced expression of integrin alpha5. RT-PCR and Western blot analysis showed that E-cadherin, regulating cell adhesion and contact cell inhibition, was decreased by H. pylori in AGS cells. In conclusion, the increased expression of cell adhesion molecules and decrease in E-cadherin expression by H. pylori might contribute to cell adhesion, invasion and possibly cell proliferation in gastric epithelial cells.
authors.affiliation: Department of Pharmacology and Institute of Gastroenterology, Brain Korea 21 Project for Medical Sciences, Yonsei University College of Medicine, Seoul 120-752, South Korea.
authors.forename: Joo Weon
authors.initials: JW
authors.lastname: Lim
authors.forename: Hyeyoung
authors.initials: H
authors.lastname: Kim
authors.forename: Kyung Hwan
authors.initials: KH
authors.lastname: Kim
mesh_terms: D000230:Adenocarcinoma / Q000209:etiology / Q000235:genetics* / Q000378:metabolism; D000446:Aldehyde-Lyases / Q000235:genetics / Q000378:metabolism; D015820:Cadherins / Q000235:genetics / Q000378:metabolism; D002448:Cell Adhesion / Q000235:genetics; D015536:Down-Regulation; D004847:Epithelial Cells / Q000378:metabolism / Q000382:microbiology; D037161:Galectins / Q000235:genetics / Q000378:metabolism; D005753:Gastric Mucosa / Q000378:metabolism / Q000382:microbiology; D005786:Gene Expression Regulation; D016481:Helicobacter Infections / Q000150:complications / Q000235:genetics* / Q000378:metabolism; D016480:Helicobacter pylori / Q000235:genetics*; D018398:Homeodomain Proteins / Q000235:genetics / Q000378:metabolism; D006801:Humans; D039564:Integrin alphaV / Q000235:genetics / Q000378:metabolism; D060588:LIM Domain Proteins; D013274:Stomach Neoplasms / Q000209:etiology / Q000235:genetics* / Q000378:metabolism; D014157:Transcription Factors / Q000235:genetics / Q000378:metabolism; D014407:Tumor Cells, Cultured; D015854:Up-Regulation
chemical_list: D015820:Cadherins; D037161:Galectins; D018398:Homeodomain Proteins; D039564:Integrin alphaV; D060588:LIM Domain Proteins; C116184:LMO7 protein, human; D014157:Transcription Factors; D000446:Aldehyde-Lyases