Yong-Li Yao1, Bo Xu, Yu-Gang Song, Wan-Dai Zhang. 1. Institute of Gastrointestinal Diseases, Nanfang Hospital, First Military Medical University, Guangzhou 510515, Guangdong Province, China. xbyyl@fimmu.edu.cn
Abstract
AIM: To explore dysregulation of cyclin E in malignancies, and to further investigate the role of cyclin E in Helicobacter pylori (H. pylori)-induced gastric precancerosis. METHODS: Four-week-old specific pathogen-free male Mongolian gerbils were employed in the study. 0.5 mL 1 x 10(8) cfu x L(-1) suspension of H.pylori NTCC11637 in Brucella broth was inoculated orally into each of 20 Mongolian gerbils, and a further 20 gerbils were inoculated with Brucella broth as controls. 10 of the infected gerbils and 10 of the non-infected control gerbils were sacrificed at 25, 45 wk after infection. The expression of cyclin E was analyzed by RT-PCR and immunohistochemical studies with monoclonal antibody to cyclin E in Mongolian gerbil of H. pylori-induced gastric precancerosis. RESULTS: H. pylori was constantly detected in all infected animals throughout the study. At 25 wk after infection of H. pylori, ulcers were observed in the antral and body of stomach (n=6). Histological examination showed that all animals developed severe inflammation and multifocal lymphoid follicles appeared in the lamina propria and submucosa of gastric antrum. At 45 wk after infection of H. pylori, severe atrophic gastritis (n=10), intestinal metaplasia (n=8) and dysplasia (n=6) could be observed. Cyclin E mRNA levels were significantly more at 25 wk after infection of H. pylori (1.27+/-0.26), and at 45 wk after infection of H. pylori (1.82+/-0.39) than control-animals (0.59+/-0.20, P<0.01) cyclin E mRNA levels were evaluated by 2.2-fold at 25 wk (P<0.01) and 3.1-fold at 45 wk (P<0.01) precancerosis induced by H. pylori, when compared with control gastric epithelium of Mongolian gerbil. Immunohistochemical staining revealed exclusive nuclear staining of cyclin E. Furthermore, there was a sequential increase in cyclin E positive cells from normal epithelium to precancerosis. CONCLUSION: Overexpression of cyclin E occurs relatively early in gastric tumorigenesis in this model.
AIM: To explore dysregulation of cyclin E in malignancies, and to further investigate the role of cyclin E in Helicobacter pylori (H. pylori)-induced gastric precancerosis. METHODS: Four-week-old specific pathogen-free male Mongolian gerbils were employed in the study. 0.5 mL 1 x 10(8) cfu x L(-1) suspension of H.pylori NTCC11637 in Brucella broth was inoculated orally into each of 20 Mongolian gerbils, and a further 20 gerbils were inoculated with Brucella broth as controls. 10 of the infected gerbils and 10 of the non-infected control gerbils were sacrificed at 25, 45 wk after infection. The expression of cyclin E was analyzed by RT-PCR and immunohistochemical studies with monoclonal antibody to cyclin E in Mongolian gerbil of H. pylori-induced gastric precancerosis. RESULTS:H. pylori was constantly detected in all infected animals throughout the study. At 25 wk after infection of H. pylori, ulcers were observed in the antral and body of stomach (n=6). Histological examination showed that all animals developed severe inflammation and multifocal lymphoid follicles appeared in the lamina propria and submucosa of gastric antrum. At 45 wk after infection of H. pylori, severe atrophic gastritis (n=10), intestinal metaplasia (n=8) and dysplasia (n=6) could be observed. Cyclin E mRNA levels were significantly more at 25 wk after infection of H. pylori (1.27+/-0.26), and at 45 wk after infection of H. pylori (1.82+/-0.39) than control-animals (0.59+/-0.20, P<0.01) cyclin E mRNA levels were evaluated by 2.2-fold at 25 wk (P<0.01) and 3.1-fold at 45 wk (P<0.01) precancerosis induced by H. pylori, when compared with control gastric epithelium of Mongolian gerbil. Immunohistochemical staining revealed exclusive nuclear staining of cyclin E. Furthermore, there was a sequential increase in cyclin E positive cells from normal epithelium to precancerosis. CONCLUSION: Overexpression of cyclin E occurs relatively early in gastric tumorigenesis in this model.
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