Helicobacter pylori -induced apoptosis in gastric epithelial cells is blocked by protein kinase C activation

Microb Pathog. 2002 Oct;33(4):167-75.


Apoptosis plays a major role in gastrointestinal epithelial cell turnover. We have examined induction of apoptosis by Helicobacter pylori in gastric AGS cells and the role of protein kinase C (PKC) which has been shown to modulate programmed cell death. Incubation of AGS cells with H. pylori resulted in an activation of caspases 3 and 9 and induced programmed cell death. The PKC activator 12- O -tetradecanoylphorbol-13-acetate (TPA) caused translocation of PKC gamma, delta and var epsilon, prevented H. pylori -induced caspase activation and programmed cell death. Cocultivation of AGS cells with H. pylori resulted in a translocation of the atypical PKC isoform PKC lambda. We suggest that inhibition of H. pylori induced apoptosis by PKC activation can play a role in the process of neoplastic transformation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Apoptosis
  • Caspase 3
  • Caspase 9
  • Caspases / metabolism
  • Cell Cycle
  • Gastric Mucosa
  • Helicobacter pylori / pathogenicity*
  • Isoenzymes / physiology
  • Protein Kinase C / physiology*
  • Tetradecanoylphorbol Acetate / pharmacology
  • Tumor Cells, Cultured


  • Isoenzymes
  • Protein Kinase C
  • Caspase 3
  • Caspase 9
  • Caspases
  • Tetradecanoylphorbol Acetate