Helicobacter priori inhibits the G1 to S transition in AGS gastric epithelial cells

Haim Shirin, Emilia Mia Sordillo, Sung H. Oh, Hirofumi Yamamoto, Thomas Delohery, I. Bernard Weinstein, Steven F. Moss*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

Abstract

Infection with the bacterium Helicobacter pylori is associated epidemiologically with development of gastric cancer. To better understand the role of H. pylori in carcinogenesis, we examined the effects of H. pylori on cell cycle-related events in the AGS gastric cancer cell line. During coculture, wild-type, toxigenic, cagA-positive H. pylori induced both apoptosis and inhibition of cell cycle progression at G1-S in AGS cells. These effects were most apparent in AGS cells synchronized by serum- deprivation and then stimulated to progress through the cell cycle by refeeding. An isogenic cagA-negative mutant H. pylori, produced similar effects. In contrast to changes induced by 5-fluorouracil, the inhibition of cell cycle progression from G1 to S caused by H. pylori was not accompanied by sustained changes in p53 or p21(cip1), but was associated with reduced expression of p27(kip1) and inhibition of transcriptional activation of the serum-response element of c-fos. Our results indicate that H. pylori inhibits cell cycle progression at G1-S and induces apoptosis, associated with reduced expression of p27(kip1) in AGS gastric cancer cells. In vivo, similar effects as a result of H. pylori infection may lead to potentially deleterious compensatory hyperproliferation by nonneoplastic gastric epithelial cells.

Original languageEnglish
Pages (from-to)2277-2281
Number of pages5
JournalCancer Research
Volume59
Issue number10
StatePublished - 15 May 1999
Externally publishedYes

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