Helicobacter pylori에 감염된 위상피세포에서 Skp2의 변화 (Changes in Skp2 in Helicobacter pylori-Infected Gastric Epithelial Cells)

서지정보

· 발행기관 : 한국식품영양학회
· 수록지 정보 : 한국식품영양학회지 / 25권 / 1호 / 64 ~ 68페이지
· 저자명 : 정혜연

초록

It has been suggested that Helicobacter pylori(H. pylori) infections can promote the development and progression of gastric cancer through the modulation of cell cycle regulators such as p27Kip1 and Skp2. p27Kip1 is a cyclin-dependent kinase (CDK) inhibitor that blocks the G1/S transition necessary for cell cycle progression. Skp2 is a component of the ubiquitin ligase complex called SCFSkp2(SKP1-Cullin-F-box), which specifically binds and promotes the degradation of p27Kip1. A low level of p27Kip1 and a high level of Skp2 have been reported in many types of cancers, including gastric cancer. In addition,a decrease in p27Kip1 has been reported in H. pylori-infected specimens. However, data on Skp2 in H. pylori infections are limited. This study examines the changes in the status of Skp2 in H. pylori-infected gastric epithelial AGS cells. For this, we stimulated AGS cells with H. pylori(NCTC 11637) at the ratio of 300:1(bacterium:cell) for 6 hours. The results of an immunoprecipitation analysis, followed by a western blot, indicate that the interaction between Skp2 and 14-3-3 was elevated 3 hours after the H. pylori treatment. In addition, there was an increase in cytoplasmic Skp2 after 3 hours, whereas there was no change in the nuclear level. Since it has been reported that interaction with 14-3-3 and the subsequent cytoplasmic translocation of Skp2 can increase its protein stability, increases in the interaction with 14-3-3 and the cytoplasmic Skp2 after the H. pylori treatment can increase the level of Skp2 in AGS cells. This phenomenon may explain,at least to some extent, the mechanism underlying the relationship between H. pylori infections and gastric carcinogenesis.

영어초록

It has been suggested that Helicobacter pylori(H. pylori) infections can promote the development and progression of gastric cancer through the modulation of cell cycle regulators such as p27Kip1 and Skp2. p27Kip1 is a cyclin-dependent kinase (CDK) inhibitor that blocks the G1/S transition necessary for cell cycle progression. Skp2 is a component of the ubiquitin ligase complex called SCFSkp2(SKP1-Cullin-F-box), which specifically binds and promotes the degradation of p27Kip1. A low level of p27Kip1 and a high level of Skp2 have been reported in many types of cancers, including gastric cancer. In addition,a decrease in p27Kip1 has been reported in H. pylori-infected specimens. However, data on Skp2 in H. pylori infections are limited. This study examines the changes in the status of Skp2 in H. pylori-infected gastric epithelial AGS cells. For this, we stimulated AGS cells with H. pylori(NCTC 11637) at the ratio of 300:1(bacterium:cell) for 6 hours. The results of an immunoprecipitation analysis, followed by a western blot, indicate that the interaction between Skp2 and 14-3-3 was elevated 3 hours after the H. pylori treatment. In addition, there was an increase in cytoplasmic Skp2 after 3 hours, whereas there was no change in the nuclear level. Since it has been reported that interaction with 14-3-3 and the subsequent cytoplasmic translocation of Skp2 can increase its protein stability, increases in the interaction with 14-3-3 and the cytoplasmic Skp2 after the H. pylori treatment can increase the level of Skp2 in AGS cells. This phenomenon may explain,at least to some extent, the mechanism underlying the relationship between H. pylori infections and gastric carcinogenesis.

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