Cell adhesion-related gene expression by Helicobacter pylori in gastric epithelial AGS cells

Joo Weon Lim, Hyeyoung Kim, Kyung Hwan Kim

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67 Citations (Scopus)


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 α5, 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 α5, 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 α5. 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.

Original languageEnglish
Pages (from-to)1284-1296
Number of pages13
JournalInternational Journal of Biochemistry and Cell Biology
Issue number8
Publication statusPublished - 2003 Aug 1

Bibliographical note

Funding Information:
This study was supported by Grant 02-PJ1-PG3-21499-0006 from the Korean Ministry of Health and Welfare (to K.H. Kim).

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Cell Biology


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