Deoxycholic Acid Could Induce Apoptosis and Trigger Gastric Carcinogenesis on Gastric Epithelial Cells by Quantitative Proteomic Analysis
Background. Pathologic duodenogastric reflux can induce or aggravate gastritis because of the presence of bile acids. Bile reflux has been generally considered to be associated with intestinal metaplasia and gastric cancer. However, the pathogenic mechanisms of the effects of bile acids on gastric m...
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| Format: | Article |
| Language: | English |
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Wiley
2016-01-01
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| Series: | Gastroenterology Research and Practice |
| Online Access: | http://dx.doi.org/10.1155/2016/9638963 |
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| author | Yanyan Shi Ying Wei Ting Zhang Jing Zhang Ye Wang Shigang Ding |
| author_facet | Yanyan Shi Ying Wei Ting Zhang Jing Zhang Ye Wang Shigang Ding |
| author_sort | Yanyan Shi |
| collection | DOAJ |
| description | Background. Pathologic duodenogastric reflux can induce or aggravate gastritis because of the presence of bile acids. Bile reflux has been generally considered to be associated with intestinal metaplasia and gastric cancer. However, the pathogenic mechanisms of the effects of bile acids on gastric mucosa are still unknown. Methods. To explore the mechanisms by which bile acids induce gastric mucosal lesions, we examined cell apoptosis in the gastric epithelial cell line GES-1 and investigated the changes in protein profiles of GES-1 cells in response to a bile acid deoxycholic acid using a proteomics approach. Changes in the profiles of the differently expressed proteins were analyzed using the DAVID and STRING programs. Results. We found apoptosis was significantly induced in GES-1 cells by deoxycholic acid. Using liquid chromatographic/tandem mass spectrometric (LC-MS/MS) methods, 134 upregulated proteins and 214 downregulated proteins were identified in the bile acid treated GES-1 cells. Bioinformatics analysis revealed the interactions and signaling networks of these differentially expressed proteins. Conclusion. These findings may improve the understanding of the molecular mechanisms underlying the pathogenicity of bile acids on gastric mucosa. |
| format | Article |
| id | doaj-art-63184249471a40249de6e7f01d441ff1 |
| institution | Kabale University |
| issn | 1687-6121 1687-630X |
| language | English |
| publishDate | 2016-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Gastroenterology Research and Practice |
| spelling | doaj-art-63184249471a40249de6e7f01d441ff12025-02-03T01:33:14ZengWileyGastroenterology Research and Practice1687-61211687-630X2016-01-01201610.1155/2016/96389639638963Deoxycholic Acid Could Induce Apoptosis and Trigger Gastric Carcinogenesis on Gastric Epithelial Cells by Quantitative Proteomic AnalysisYanyan Shi0Ying Wei1Ting Zhang2Jing Zhang3Ye Wang4Shigang Ding5Research Center of Clinical Epidemiology, Peking University Third Hospital, Beijing 100191, ChinaDepartment of Gastroenterology, Peking University Third Hospital, Beijing 100191, ChinaDepartment of Microbiology, Peking University Health Science Center, Beijing 100191, ChinaDepartment of Gastroenterology, Peking University Third Hospital, Beijing 100191, ChinaDepartment of Gastroenterology, Peking University Third Hospital, Beijing 100191, ChinaDepartment of Gastroenterology, Peking University Third Hospital, Beijing 100191, ChinaBackground. Pathologic duodenogastric reflux can induce or aggravate gastritis because of the presence of bile acids. Bile reflux has been generally considered to be associated with intestinal metaplasia and gastric cancer. However, the pathogenic mechanisms of the effects of bile acids on gastric mucosa are still unknown. Methods. To explore the mechanisms by which bile acids induce gastric mucosal lesions, we examined cell apoptosis in the gastric epithelial cell line GES-1 and investigated the changes in protein profiles of GES-1 cells in response to a bile acid deoxycholic acid using a proteomics approach. Changes in the profiles of the differently expressed proteins were analyzed using the DAVID and STRING programs. Results. We found apoptosis was significantly induced in GES-1 cells by deoxycholic acid. Using liquid chromatographic/tandem mass spectrometric (LC-MS/MS) methods, 134 upregulated proteins and 214 downregulated proteins were identified in the bile acid treated GES-1 cells. Bioinformatics analysis revealed the interactions and signaling networks of these differentially expressed proteins. Conclusion. These findings may improve the understanding of the molecular mechanisms underlying the pathogenicity of bile acids on gastric mucosa.http://dx.doi.org/10.1155/2016/9638963 |
| spellingShingle | Yanyan Shi Ying Wei Ting Zhang Jing Zhang Ye Wang Shigang Ding Deoxycholic Acid Could Induce Apoptosis and Trigger Gastric Carcinogenesis on Gastric Epithelial Cells by Quantitative Proteomic Analysis Gastroenterology Research and Practice |
| title | Deoxycholic Acid Could Induce Apoptosis and Trigger Gastric Carcinogenesis on Gastric Epithelial Cells by Quantitative Proteomic Analysis |
| title_full | Deoxycholic Acid Could Induce Apoptosis and Trigger Gastric Carcinogenesis on Gastric Epithelial Cells by Quantitative Proteomic Analysis |
| title_fullStr | Deoxycholic Acid Could Induce Apoptosis and Trigger Gastric Carcinogenesis on Gastric Epithelial Cells by Quantitative Proteomic Analysis |
| title_full_unstemmed | Deoxycholic Acid Could Induce Apoptosis and Trigger Gastric Carcinogenesis on Gastric Epithelial Cells by Quantitative Proteomic Analysis |
| title_short | Deoxycholic Acid Could Induce Apoptosis and Trigger Gastric Carcinogenesis on Gastric Epithelial Cells by Quantitative Proteomic Analysis |
| title_sort | deoxycholic acid could induce apoptosis and trigger gastric carcinogenesis on gastric epithelial cells by quantitative proteomic analysis |
| url | http://dx.doi.org/10.1155/2016/9638963 |
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