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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Yoshida-moriguchi, Takako De Bernabé, Daniel Beltrán-valero Harper, Hollie A. Inamori, Kei-ichiro Henry, Michael D. Campbell, Kevin P. Weydert, Christine J. Willer, Tobias |
| Description | Author Affiliation: de Bernabé DB ( Howard Hughes Medical Institute, University of Iowa, Roy J. and Lucille A. Carver College of Medicine, Iowa City, Iowa 52242-1101, USA.) |
| Abstract | The interaction between epithelial cells and the extracellular matrix is crucial for tissue architecture and function and is compromised during cancer progression. Dystroglycan is a membrane receptor that mediates interactions between cells and basement membranes in various epithelia. In many epithelium-derived cancers, β-dystroglycan is expressed, but α-dystroglycan is not detected. Here we report that α-dystroglycan is correctly expressed and trafficked to the cell membrane but lacks laminin binding as a result of the silencing of the like-acetylglucosaminyltransferase (LARGE) gene in a cohort of highly metastatic epithelial cell lines derived from breast, cervical, and lung cancers. Exogenous expression of LARGE in these cancer cells restores the normal glycosylation and laminin binding of α-dystroglycan, leading to enhanced cell adhesion and reduced cell migration in vitro. Our findings demonstrate that LARGE repression is responsible for the defects in dystroglycan-mediated cell adhesion that are observed in epithelium-derived cancer cells and point to a defect of dystroglycan glycosylation as a factor in cancer progression. |
| ISSN | 00219258 |
| e-ISSN | 1083351X |
| Journal | Journal of Biological Chemistry |
| Issue Number | 17 |
| Volume Number | 284 |
| Language | English |
| Publisher | American Society for Biochemistry and Molecular Biology (United States) |
| Publisher Date | 2009-04-24 |
| Publisher Place | United States |
| Access Restriction | Open |
| Subject Keyword | Dystroglycans Metabolism Epithelium Pathology Gene Expression Regulation, Neoplastic Laminin N-Acetylglucosaminyltransferases Skin Neoplasms Cell Adhesion Cell Line, Tumor Gene Silencing Glycosylation HeLa Cells Models, Biological Neoplasm Metastasis Protein Binding Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't Biochemistry Molecular Biology |
| Content Type | Text |
| Resource Type | Article |
| Subject | Cell Biology Biochemistry Molecular Biology |
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