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FAM60A,increased by Helicobacter pylori,promotes proliferation and suppresses apoptosis of gastric cancer cells by targeting the PI3K/AKT pathway
Institution:1. Department of Gastroenterology, Shengjing Hospital of China Medical University, Shenyang, 110004, Liaoning, China;2. Medical Research Center, Shengjing Hospital of China Medical University, Benxi, 117000, Liaoning, China;1. Department of Computer Science and Engineering, Huaqiao University, China;2. Department of Computer Science and Engineering, Harbin Institute of Technology, China;3. Oregon State University, USA;4. Department of Electronic Engineering, Columbia University, USA;5. School of Computer Science, The University of Adelaide, Australia;6. School of Information Science and Technology, Xiamen University, China;1. Key Lab of Structures Dynamic Behavior and Control of the Ministry of Education (Harbin Institute of Technology), Harbin 150090, China;2. School of Civil Engineering, Harbin Institute of Technology, Heilongjiang, Harbin 150090, China;3. School of Civil Engineering, The University of Sydney, Sydney, NSW 2006, Australia;1. Soochow University Laboratory of Cancer Molecular Genetics, Medical College of Soochow University, Suzhou, Jiangsu, 215123, China;2. Department of Genetics, School of Biology and Basic Medical Science, Medical College of Soochow University, Suzhou, Jiangsu, 215123, China;3. Department of Cardiothoracic Surgery, The First Affiliated Hospital of Soochow University, Medical College of Soochow University, Suzhou, Jiangsu, 215006, China;4. Department of Respiratory Medicine, The First Affiliated Hospital of Soochow University, Medical College of Soochow University, Suzhou, Jiangsu, 215006, China;5. Department of Thoracic Surgery, The Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, 150086, China;6. Department of Basic Medicine, Kangda College of Nanjing Medical University, Lianyungang, 222000, China;7. Suzhou Key Laboratory for Molecular Cancer Genetics, Suzhou, Jiangsu, 215123, China;1. School of Civil Engineering, Shenyang Jianzhu University, Shenyang 110168, China;2. Key Lab of Structures Dynamic Behaviour and Control of the Ministry of Education, Harbin Institute of Technology, Harbin 150090, China;3. School of Civil Engineering, Liaoning Technical University, Fuxin 123000, China;4. School of Material Science and Engineering, Shenyang Jianzhu University, Shenyang 110168, China
Abstract:Helicobacter pylori (H. pylori) infection can promote the development of gastric cancer (GC); however, the underlying mechanism is not clear. FAM60A has been found showing high levels in some cancer cells, including lung cancer (A549), and pancreatic cancer (Capan-2) cell lines. Data in oncomine showed that FAM60A overexpression was an critical prognostic factor in GC. In this study, we showed that knockdown of FAM60A could revert the increase of proliferation and the decrease of apoptosis caused by H.pylori infection in HGC-27 and AGS cells. Conversely, FAM60A upregulation promoted proliferation and inhibited apoptosis in HGC-27 and AGS cells. We also found that the PI3K/AKT pathway inhibitor LY294002 could revert the changes caused by FAM60A upregulation in HGC-27 and AGS cells. Thus, our study provides evidence that FAM60A act as a carcinogen and suggests that H. pylori-induced upregulation of FAM60A may contribute to the development of gastric cancer.
Keywords:FAM60A  H  pylori  Gastric cancer  Cell proliferation  Cell apoptosis  AKT
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