Journal
CELLULAR MICROBIOLOGY
Volume 8, Issue 11, Pages 1740-1752Publisher
BLACKWELL PUBLISHING
DOI: 10.1111/j.1462-5822.2006.00743.x
Keywords
-
Categories
Ask authors/readers for more resources
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 cagA mutant. AP1 and cAMP response element (CRE), but not NF-kappa B, 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.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available