1. Sustained Exposure to Helicobacter pylori Lysate Inhibits Apoptosis and Autophagy of Gastric Epithelial Cells
- Author
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Xueyun Huo, Wang Cunlong, Jin Xing, Changlong Li, Xin Liu, Xiulin Zhang, Zhenwen Chen, Jing Lu, Meng Guo, Jianyi Lv, Xiaoyan Du, Yang He, and Xuancheng Lu
- Subjects
0301 basic medicine ,autophagy ,Cancer Research ,Cell ,Biology ,medicine.disease_cause ,lcsh:RC254-282 ,gastric epithelial cell ,03 medical and health sciences ,0302 clinical medicine ,medicine ,Original Research ,Helicobacter pylori ,Autophagy ,apoptosis ,lcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens ,biology.organism_classification ,030104 developmental biology ,medicine.anatomical_structure ,Oncology ,Cell culture ,Apoptosis ,030220 oncology & carcinogenesis ,FOXO4 ,Cancer research ,Signal transduction ,Carcinogenesis ,carcinogenesis - Abstract
Helicobacter pylori is designated as a class I carcinogen of human gastric cancer following long-term infection. During this process, H. pylori bacteria persist in proliferation and death, and release bacterial components that come into contact with gastric epithelial cells and regulate host cell function. However, the impact of long-term exposure to H. pylori lysate on the pathological changes of gastric cells is not clear. In this study, we aimed to investigate the regulation and mechanisms involved in gastric cell dysfunction following continuous exposure to H. pylori lysate. We co-cultured gastric cell lines GES-1 and MKN-45 with H. pylori lysate for 30 generations, and we found that sustained exposure to H. pylori lysate inhibited GES-1 cell invasion, migration, autophagy, and apoptosis, while it did not inhibit MKN-45 cell invasion or migration. Furthermore, Mongolian gerbils infected with H. pylori ATCC 43504 strains for 90 weeks confirmed the in vitro results. The clinical and in vitro data indicated that sustained exposure to H. pylori lysate inhibited cell apoptosis and autophagy through the Nod1-NF-κB/MAPK-ERK/FOXO4 signaling pathway. In conclusion, sustained exposure to H. pylori lysate promoted proliferation of gastric epithelial cells and inhibited autophagy and apoptosis via Nod1-NF-κB/MAPK-ERK/FOXO4 signaling pathway. In the process of H. pylori-induced gastric lesions, H. pylori lysate plays as an “accomplice” to carcinogenesis.
- Published
- 2020