Helicobacter pylori inhibits gastric cell cycle progression

Amel Ahmed, Duane Smoot, George Littleton, Robert Tackey, Curla S. Walters, Fatah Kashanchi, Cornell R. Allen, Hassan Ashktorab

Research output: Contribution to journalArticlepeer-review

42 Scopus citations


Helicobacter pylori infection of the gastric mucosa is associated with changes in gastric epithelial cell proliferation. In vitro studies have shown that exposure to H. pylori inhibits proliferation of gastric cells. This study sought to investigate the cell cycle progression of gastric epithelial cell lines in the presence and absence of H. pylori. Unsynchronized and synchronized gastric epithelial cell lines AGS and KatoIII were exposed to H. pylori over a 24-h period. Cell cycle progression was determined by flow cytometry using propidium iodide (PI), and by analysis of cyclin E, p21, and p53 protein expression using Western blots. In the absence of H. pylori 40, 45, and 15% of unsynchronized AGS cells were in G0-G1, S, and G2-M phases, respectively, by flow cytometry analysis. When AGS cells were cultured in the presence of H. pylori, the S phase decreased 10% and the G0-G1 phase increased 17% after 24 h compared with the controls. KatoIII cells, which have a deleted p53 gene, showed little or no response to H. pylori. When G1/S synchronized AGS cells were incubated with media containing H. pylori, the G1 phase increased significantly (25%, P < 0.05) compared with controls after 24 h. In contrast, the control cells were able to pass through S phase. The inhibitory effects of H. pylori on the cell cycle of AGS cells were associated with a significant increase in p53 and p21 expression after 24 h. The expression ofcyclin E was downregulated in AGS cells following exposure of AGS cells to H. pylori for 24 h. This study shows that H. pylori-induced growth inhibition in vitro is predominately at the G0-G1 checkpoint. Our results suggest that p53 may be important in H. pylori-induced cell cycle arrest. These results support a role for cyclin-dependent kinase inhibitors in the G1 cell cycle arrest exerted by H. pylori and its involvement in changing the regulatory proteins, p53, p21, and cyclin E in the cell cycle. (C) 2000 Editions scientifiques et medicales Elsevier SAS.

Original languageEnglish (US)
Pages (from-to)1159-1169
Number of pages11
JournalMicrobes and Infection
Issue number10
StatePublished - 2000
Externally publishedYes


  • Cell cycle arrest
  • Cyclin E
  • Gastric epithelial cells
  • Helicobacteri pylori
  • p21
  • p53

ASJC Scopus subject areas

  • Microbiology
  • Immunology
  • Infectious Diseases


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