摘要
目的研究PKC同工酶在H.pylori感染引起胃癌发生中起作用。方法将幽门螺杆菌和人胃上皮腺癌细胞系AGS细胞共培养(细菌∶细胞=200∶1),在幽门螺杆菌攻击AGS细胞后的0h、0.5h、1h、4h、6h、12h、24h时间点分别提取AGS细胞的总RNA,同时提取相对应时间点平行培养的未受幽门螺杆菌攻击的AGS细胞的总RNA作为对照组,以Beta-actin为内参照,应用Taq-Man实时荧光定量RT-PCR技术研究这些样品的PKC同工酶的mRNA变化情况。结果与对照组相比,PKCε、PKCγ、PKCι、PKCζ、PKCα mRNA水平呈现增高趋势;PKCθ mRNA水平呈现持续下降趋势;PKCδ mRNA水平与对照组呈现一致表达趋势。结论H.pylori可能通过上调具有肿瘤增殖活性的PKCα、ε、γ、ι、ζ,下调了具有凋亡活性的PKCθ,参与H.pylori引起胃癌的发生过程。H.pylori对PKCδ mRNA水平没有影响。
Objective To explore the effect of PKC isoenzymes in H pylori related gastric cancer. Methods The AGS human gastric epithelial adenocarcinoma cell line was cocuhured with H. pylori （ bacteria ： cell = 200 ： 1 ）. Total RNA was extracted from Hpylori treated AGS cells at 0 h, 0.5 h, 1 h, 4 h, 6 h, 12 h, 24 h, 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 Compared with control groups, PKCε、PKCγ、PKCι、PKCζ、PKCα mRNA level showed remarkably ascending tendency, while PKC θ mRNA level displayed remarkably descending tendency. Regardless of H. pylori treated or control groups, PKCδ mRNA level was no difference. Conclusion H. pylori may take part in the process of gastric cancer induced by H. pylori through up-regulating of PKCα、ε、γ、ι and ζ,,which have the effect of regulating tumor proliferation, function and down-regulating PKCθ, which has the effect of apoptosis function. H. pylori may have no effect on PKCδ in AGS.
出处
《胃肠病学和肝病学杂志》
CAS
2007年第3期280-283,共4页
Chinese Journal of Gastroenterology and Hepatology
基金
中国国家自然科学基金(30370078)
