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| Type |
Poster Presentation |
| Area |
Analytical Chemistry |
| Room No. |
Exhibition Hall 2 |
| Time |
4월 19일 (금요일) 11:00~12:30 |
| Code |
ANAL.P-285 |
| Subject |
Proteogenomic analysis of diffuse-type gastric carcinogenesis induced by E-cadherin, p53, and Smad4 loss in mice |
| Authors |
Jingi Bae, Su-Jin Kim, Sang-Won Lee*
Department of Chemistry, Korea University, Korea
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| Abstract |
ic cancer (GC) is the second most common cause of cancer related deaths worldwide, which can be divided into adenocarcinomas of the diffuse and the intestinal type according to the Lauren classification. A recently study reported the establishment of the Pdx-1-Cre;Cdh1F/+;Trp53F/F;Smad4F/F (pChePS) mouse model, which spontaneously generates metastatic gastric tumors that closely recapitulate human diffuse-type gastric cancer (DGC). An interesting feature of this model is that the developed DGCs display a near-complete loss of E-cadherin expression (encoded by Cdh1).
In order to investigate the functional cooperation of Smad4, p53, and E-cadherin loss in DGC carcinogenesis at the molecular level and to delineate the mechanism of Cdh1 repression, we performed a proteogenomic analysis.
In this study, we identified 145,816 peptides and 7,058 unique proteins by using Uniprot DB with MS-GF+ search engine. The in-depth quantitative proteomic analysis identified in 1448 differentially expressed proteins (|DEPs| ≥ 2 FC) in DGCs when compared to normal gastric epithelium (NGE).
Through a series of comprehensive proteogenomic analyses of our unique mouse models, we have uncovered important pathways and key mediators involved in DGC carcinogenesis. We suggest promising target molecules in DGC carcinogenesis, including Spp1 and its downstream effector Bcl-xL. Moreover, we identified Tβ4 and Zeb2 as important potential repressors of E-cadherin in DGC carcinogenesis.
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| E-mail |
bjg0926@nate.com |
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123rd General Meeting of the KCS