Phosphorylation and inactivation of PTEN at residues Ser380/Thr382/383 induced by Helicobacter pylori promotes gastric epithelial cell survival through PI3K/Akt pathway |
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| Authors: | Zhen Yang Chuan Xie Wenting Xu Gongmeizi Liu Ximei Cao Wei Li Jiang Chen Yin Zhu Shiwen Luo Zhijun Luo Nonghua Lu |
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| Affiliation: | 1. Department of Gastroenterology, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, China;2. Center for Experimental Medicine, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, China;3. The Medical College of Nanchang University, Nanchang, Jiangxi, China;4. Department of Biochemistry, Boston University School of Medicine, Boston, MA, USA |
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| Abstract: | ![]()
Phosphorylation of PTEN at residues Ser380/Thr382/383 leads to loss of phosphatase activity and tumor suppressor function. Here, we found that phosphorylation of PTEN at residues Ser380/Thr382/383 was increased with gastric carcinogenesis, and more importantly, Helicobacter pylori was a trigger of this modification in chronic non-atrophic gastritis. H. pylori could phosphorylate and inactivate PTEN in vivo and in vitro, resulting in survival of gastric epithelial cells. Furthermore, stable expression of dominant-negative mutant PTEN or inhibition of Akt prevented the enhanced survival induced by H. pylori. These results indicate that PTEN phosphorylation at residues Ser380/Thr382/383 is a novel mechanism of PTEN inactivation in gastric carcinogenesis, and H. pylori triggers this modification, resulting in activation of the PI3K/Akt pathway and promotion of cell survival. |
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| Keywords: | gastric carcinogenesis Helicobacter pylori phosphatase and tensin homolog phosphorylation PI3K/Akt pathway |
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