| AIM:Helicobacter pylori infects about 50% of the world's population and has been shown to be an important pathogen in several digestive disorders, such as peptic ulcers, chronic gastritis, and gastric cancer. Epidemiologic studies have shown that H. pylori infection is a risk factor for gastric carcinoma, and H. pylori has been classified by the World Health Organization as a group 1 carcinogen. Protein kinases C (PKCs) is a family of serine/threonine kinases that are critical for signal transduction pathways involved in growth, differentiation and cell death. Recently, expression of PKC in gastric cancer has been studied. One investigation revealed that H. pylori infection play a part through PKC effect in the process of intestinal metaplasia, atypical hyperplasia, gastric cancer. The aim of this study was to explore in detail which PKC isoenzymes may be involved in H. pylori infection induced gastric cancer. Similar researchs have not been reported at present.METHODS: The AGS human gastric epithelial adenocarcinoma cell line was cocultured with H pylori. (bacteria :cell=200:1 ) Total RNA was extracted from H. pylori treated AGS cells at Oh, 0.5h, 1h., 4h, 6h, 12h, 24h time point , while at the same time point total RNA was also extracted from H. pylori untreated AGS cell as control. Real time quantitative reverse transcription polymerase chain reaction (RT-Q-PCR) assay was used to quantitate the mRNA level of these samples. Beta-actin was used as internal standard. RESULTS:1. PKCε, PKCγ, PKCι, PKCζmRNA displayed stable low level expression in control group, while H. pylori attacked sample, these genes' mRNA level showed marked ascending tendency. The PKCε,PKCγ,PKCι,PKCζmRNA level of 24h time point ration Oh time point separately increased 8.57 fold, 31.38 fold, 3.08 fold and 3.42 fold.2. PKCθmRNA level showed persistence descending tendency in H. pylori treated samples and its level of 24h time point ration Oh time point decreased 8.57 fold .The control group showed a tendency of Oh～1h descending 2.8 fold , 1h～12h ascending 1.7 fold and 12h～24h descending 4 fold . comparing to control group, PKCθmRNA level in H. pylori attacked samples have the down-regulate tendency in general.3. Regardless of H. pylori treated or control groups, PKCαmRNA level express the tendency of ascending. H. pylori treated samples' PKCαmRNA level of 6h time point ration Oh time point rapidly increased 6.36 fold, then maintain the high level. Control group display slowly ascending tendency, whatever H. pylori treated group and control ,the PKCαmRNA level at 24h time point was the same.4. Regardless of H. pylori treated or control groups, PKCδmRNA level appearance was with on accord.CONCLUSION:1. PKCε,PKCγ,PKCι,PKCζmRNA level displayed stable low level expression in control group, while H. pylori attacked sample, these genes' mRNA level showed marked ascending tendency. The result hints H. pylori may take part in the process of H. pylori inducing gastric cancer through up-regulating PKCε,γ,ι,ζwhich have the effect of regulating tumor proliferation function.2. PKCθmRNA level was not stable expressed in control group, this may indicate PKCθtake part in AGS cell proliferation and apoptosis. Comparing to control group, PKCθmRNA level in H. pylori attacked samples have the down-regulate tendency in general. This may manifest H. pylori may take part in the process of H, pylori inducing gastric cancer through down-regulating PKCθwhich have the effect of regulating apoptosis function.3. Regardless of H, pylori treated or control groups, PKCαmRNA level express the tendency of ascending, this indicates PKCαtake part in AGS cell proliferation in common cultured circumstance. H. pylori can accelerate PKCαmRNA level to a high level in advance.4. Regardless of H pylori treated or control groups, PKCδmRNA level appearance was with on accord . H. pylori may have no effect on PKCδin AGS.
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