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

Biochem Biophys Res Commun. 2003 Nov 28;311(4):809-14. doi: 10.1016/j.bbrc.2003.10.077.

Abstract

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.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adenocarcinoma / genetics
  • Adenocarcinoma / metabolism
  • Adenocarcinoma / pathology
  • Angiogenesis Inducing Agents / metabolism
  • Carcinoma, Adenosquamous / genetics
  • Carcinoma, Adenosquamous / metabolism
  • Carcinoma, Adenosquamous / pathology
  • Cell Line, Tumor
  • Collagenases / biosynthesis
  • Endopeptidases / genetics*
  • Gene Expression Regulation, Bacterial / genetics*
  • Helicobacter Infections / complications
  • Helicobacter Infections / genetics*
  • Helicobacter pylori / genetics*
  • Humans
  • Neovascularization, Pathologic / genetics*
  • Stomach Neoplasms / etiology
  • Stomach Neoplasms / genetics*
  • Stomach Neoplasms / metabolism
  • Stomach Neoplasms / pathology*

Substances

  • Angiogenesis Inducing Agents
  • Endopeptidases
  • Collagenases