Mechanisms for Helicobacter pylori CagA-induced cyclin D1 expression that affect cell cycle

Ya Jen Chang, Ming Shiang Wu, Jaw Town Lin, Richard G. Pestell, Martin J. Blaser, Ching Chow Chen

Research output: Contribution to journalArticlepeer-review

45 Scopus citations


Particular Helicobacter pylori genotypes differentially induce epithelial cell proliferation, but the mechanisms are not characterized. We explored the effect of H.pylori CagA on expression of cyclin D1, an important cell cycle regulator. H.pylori-induced cell survival and cyclin D1 expression were attenuated in a c agA mutant. AP1 and cAMP response element (CRE), but not NF-κB, were involved in the induced cyclin D1 expression. Diminished mitogen-activated protein kinase (MAPK) activation, especially involving p38, with downstream effects on AP1 and CRE activation, was observed for the cagA mutant. In total, these data show that cagA+ H.pylori strains are enhanced in their ability to activate MAPKs and downstream transcription factors, increasing cyclin D1 expression, G1-S phase progression, and host cell survival, explaining both the preferential survival of affected host cells, and the enhanced oncogenesis by these bacteria.

Original languageEnglish (US)
Pages (from-to)1740-1752
Number of pages13
JournalCellular Microbiology
Issue number11
StatePublished - Nov 2006
Externally publishedYes

All Science Journal Classification (ASJC) codes

  • Microbiology
  • Immunology
  • Virology

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