https://scholars.lib.ntu.edu.tw/handle/123456789/461713
標題: | Deletion of cadherin-17 enhances intestinal permeability and susceptibility to intestinal tumour formation | 作者: | Chang Y.-Y. LINDA CHIA-HUI YU Yu I.-S. Jhuang Y.-L. Huang W.-J. CHING-YAO YANG YUNG-MING JENG |
公開日期: | 2018 | 出版社: | John Wiley and Sons Ltd | 卷: | 246 | 期: | 3 | 起(迄)頁: | 289-299 | 來源出版物: | Journal of Pathology | 摘要: | Cadherin-17 is an adhesion molecule expressed specifically in intestinal epithelial cells. It is frequently underexpressed in human colorectal cancer. The physiological function of cadherin-17 and its role in tumourigenesis have not yet been determined. We used the transcription activator-like effector nuclease technique to generate a Cdh17 knockout (KO) mouse model. Intestinal tissues were analysed with histological, immunohistochemical and ultrastructural methods. Colitis was induced by oral administration of dextran sulphate sodium (DSS), and, to study effects on intestinal tumourigenesis, mice were given azoxymethane (AOM) and DSS to induce colitis-associated cancer. Cdh17 KO mice were viable and fertile. The histology of their small and large intestines was similar to that of wild-type mice. The junctional architecture of the intestinal epithelium was preserved. The loss of cadherin-17 resulted in increased permeability and susceptibility to DSS-induced colitis. The AOM/DSS model demonstrated that Cdh17 KO enhanced tumour formation and progression in the intestine. Increased nuclear translocation of Yap1, but not of β-catenin, was identified in the tumours of Cdh17 KO mice. In conclusion, cadherin-17 plays a crucial role in intestinal homeostasis by limiting the permeability of the intestinal epithelium. Cadherin-17 is also a tumour suppressor for intestinal epithelia. Copyright ? 2018 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd. Copyright ? 2018 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd. |
URI: | https://www.scopus.com/inward/record.uri?eid=2-s2.0-85053725713&doi=10.1002%2fpath.5138&partnerID=40&md5=cec0358450c29e4b7595f526000f4e8c https://scholars.lib.ntu.edu.tw/handle/123456789/461713 |
ISSN: | 0022-3417 | DOI: | 10.1002/path.5138 | SDG/關鍵字: | azoxymethane; cadherin; Cdh17 protein, mouse; dextran sulfate; phosphoprotein; signal transducing adaptor protein; tumor suppressor protein; Yap protein, mouse; adenoma; animal; C57BL mouse; carcinoma; colitis; colorectal tumor; disease model; gene deletion; genetic predisposition; genetics; intestine absorption; intestine mucosa; knockout mouse; metabolism; nucleocytoplasmic transport; pathology; permeability; phenotype; signal transduction; Active Transport, Cell Nucleus; Adaptor Proteins, Signal Transducing; Adenoma; Animals; Azoxymethane; Cadherins; Carcinoma; Colitis; Colorectal Neoplasms; Dextran Sulfate; Disease Models, Animal; Gene Deletion; Genetic Predisposition to Disease; Intestinal Absorption; Intestinal Mucosa; Mice, Inbred C57BL; Mice, Knockout; Permeability; Phenotype; Phosphoproteins; Signal Transduction; Tumor Suppressor Proteins |
顯示於: | 醫學系 |
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