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Molecular & Cellular Proteomics 5:702-713, 2006.
© 2006 by The American Society for Biochemistry and Molecular Biology, Inc.

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Research

Subcellular and Functional Proteomic Analysis of the Cellular Responses Induced by Helicobacter pylori^*,S

Chia-Hsin Chan, Chia-Cheng Ko, Jan-Gowth Chang, Sung-Fang Chen^¶, Ming-Shiang Wu^||, Jaw-Town Lin^|| and Lu-Ping Chow^,**,

From the Graduate Institute of Biochemistry and Molecular Biology, College of Medicine, National Taiwan University, Taipei 100, Taiwan, Department of Molecular Medicine, China Medical University Hospital, Taichung 404, Taiwan, ^¶ Department of Proteomics, Biomedical Engineering Center, Industrial Technology Research Institute, Hsinchu 310, Taiwan, and Departments of ^|| Internal Medicine and ^** Medical Genetics, National Taiwan University Hospital, Taipei 100, Taiwan

Helicobacter pylori infection is a crucial factor in the pathogenesis of several digestive disorders, including peptic ulcers, chronic gastritis, and gastric cancer. Moreover H. pylori induces disease-specific protein expression in gastric epithelial cells. The aim of the present study was to characterize proteins differentially expressed in H. pylori-infected gastric epithelial AGS cells. An in vitro model was established using a multiplicity of infection of 100 and evaluating the effectiveness of H. pylori infection by functional analyses. Changes in protein patterns were identified using a proteomic approach consisting of two-dimensional fluorescence difference gel electrophoresis and mass spectrometry. The expression of many proteins was found to be altered, and 28 of these were identified and classified as protein synthesis- and folding-related proteins, cytoskeleton proteins, metabolic enzymes, transcription- and translation-related proteins, angiogenesis/metastasis-related proteins, cell communication/signal transduction-related proteins, or others (oxygen-regulated protein and oncoprotein). The expression profiles of eight of these proteins, laminin -1 chain precursor, valosin-containing protein, heat shock 70-kDa protein, mitochondrial matrix protein P1, FK506-binding protein 4, T-complex protein 1, enolase , and 14-3-3 ß were further examined in cancerous and paired surrounding normal tissues by immunoblot assay and immunohistochemical staining to identify molecular targets that may be involved in the pathogenesis of H. pylori-induced gastric diseases. On the basis of our results, valosin-containing protein, mitochondrial matrix protein P1, T-complex protein 1, enolase , and 14-3-3 ß may play a crucial role in H. pylori-induced gastric carcinogenesis by mediating antiapoptotic and proliferative responses.

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