Helicobacter pylori infection influences expression of genes related to angiogenesis and invasion in human gastric carcinoma cells

Infection with Helicobacter pylori ( H. pylori) is considered a risk factor for gastric carcinoma. The purpose of this study was to clarify whether H. pylori infection plays a role in progression of gastric carcinoma. We examined the expression of genes encoding angiogenic factors and proteases by h...

Full description

Saved in:
Bibliographic Details
Published inBiochemical and biophysical research communications Vol. 311; no. 4; pp. 809 - 814
Main Authors Kitadai, Yasuhiko, Sasaki, Atsunori, Ito, Masanori, Tanaka, Shinji, Oue, Naohide, Yasui, Wataru, Aihara, Miki, Imagawa, Kenichi, Haruma, Ken, Chayama, Kazuaki
Format Journal Article
LanguageEnglish
Published United States Elsevier Inc 28.11.2003
Subjects
Online AccessGet full text

Cover

Loading…
More Information
Summary:Infection with Helicobacter pylori ( H. pylori) is considered a risk factor for gastric carcinoma. The purpose of this study was to clarify whether H. pylori infection plays a role in progression of gastric carcinoma. We examined the expression of genes encoding angiogenic factors and proteases by human gastric carcinoma cell lines (MKN-1 and TMK-1) co-cultured with or without H. pylori by cDNA microarray analysis. Co-culture with H. pylori increased expression of mRNAs encoding interleukin (IL)-8, vascular endothelial growth factor (VEGF), angiogenin, urokinase-type plasminogen activator (uPA), and metalloproteinase (MMP)-9 by gastric carcinoma cells. Up-regulation of these genes at the mRNA and protein levels was confirmed by Northern blot analysis, semi-quantitative RT-PCR analysis, and ELISA. In vitro angiogenic and collagenase activities of conditioned medium from the gastric carcinoma cells were also stimulated by co-culture with H. pylori. These results indicate that H. pylori infection may regulate angiogenesis and invasion of human gastric carcinoma.
Bibliography:ObjectType-Article-2
SourceType-Scholarly Journals-1
ObjectType-Feature-1
content type line 23
ObjectType-Article-1
ObjectType-Feature-2
ISSN:0006-291X
1090-2104
DOI:10.1016/j.bbrc.2003.10.077