Title Helicobacter pylori γ-Glutamyltranspeptidase Induces Cell Cycle Arrest at the G1-S Phase Transition
Author Kyung-Mi Kim1, Seung-Gyu Lee2, Jung-Min Kim1, Do-Su Kim1, Jea-Young Song1, Hyung-Lyun Kang1,3, Woo-Kon Lee1,3, Myung-Je Cho1,3, Kwang-Ho Rhee1,3, Hee-Shang Youn4, and Seung-Chul Baik1,3*
Address 1Department of Microbiology, Gyeongsang National University School of Medicine, Jinju 660-751, Republic of Korea, 2National Institute of Animal Science, RDA, Suwon 441-706, Republic of Korea, 3Research Institute of Life Science, Gyeongsang National University School of Medicine, Jinju 660-751, Republic of Korea, 4Pediatrics, Gyeongsang National University School of Medicine, Jinju 660-751, Republic of Korea
Bibliography Journal of Microbiology, 48(3),372-377, 2010,
DOI
Key Words H. pylori, γ-glutamyltranspeptidase, cell cycle
Abstract In our previous study, we showed that Helicobacter pylori γ-glutamyltranspeptidase (GGT) is associated with H. pylori-induced apoptosis through a mitochondrial pathway. To better understand the role of GGT in apoptosis, we examined the effect of GGT on cell cycle regulation in AGS cells. To determine the effect of recombinant GGT (rGGT) on cell cycle distribution and apoptosis, rGGT-treated and untreated AGS cells were analyzed in parallel by flow cytometry using propidium iodide (PI). We found that rGGT inhibited the growth of AGS cells in a time-dependent manner, and that the pre-exposure of cells to a caspase-3 inhibitor (z-DEVD-fmk) effectively blocked GGT-induced apoptosis. Cell cycle analysis showed G1 phase arrest and apoptosis in AGS cells following rGGT treatment. The rGGT-mediated G1 phase arrest was found to be associated with down-regulation of cyclin E, cyclin A, Cdk 4, and Cdk 6, and the up-regulation of the cyclindependent kinase (Cdk) inhibitors p27 and p21. Our results suggest that H. pylori GGT induces cell cycle arrest at the G1-S phase transition.