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N-Cadherin Promotes Motility in Human Breast Cancer Cells Regardless of Their E-Cadherin Expression
E-cadherin is a transmembrane glycoprotein that mediates calcium-dependent, homotypic cell–cell adhesion and plays a role in maintaining the normal phenotype of epithelial cells. Decreased expression of E-cadherin has been correlated with increased invasiveness of breast cancer. In other systems, in...
Autores principales: | , , , |
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Formato: | Texto |
Lenguaje: | English |
Publicado: |
The Rockefeller University Press
1999
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2151177/ https://www.ncbi.nlm.nih.gov/pubmed/10545506 |
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author | Nieman, Marvin T. Prudoff, Ryan S. Johnson, Keith R. Wheelock, Margaret J. |
author_facet | Nieman, Marvin T. Prudoff, Ryan S. Johnson, Keith R. Wheelock, Margaret J. |
author_sort | Nieman, Marvin T. |
collection | PubMed |
description | E-cadherin is a transmembrane glycoprotein that mediates calcium-dependent, homotypic cell–cell adhesion and plays a role in maintaining the normal phenotype of epithelial cells. Decreased expression of E-cadherin has been correlated with increased invasiveness of breast cancer. In other systems, inappropriate expression of a nonepithelial cadherin, such as N-cadherin, by an epithelial cell has been shown to downregulate E-cadherin expression and to contribute to a scattered phenotype. In this study, we explored the possibility that expression of nonepithelial cadherins may be correlated with increased motility and invasion in breast cancer cells. We show that N-cadherin promotes motility and invasion; that decreased expression of E-cadherin does not necessarily correlate with motility or invasion; that N-cadherin expression correlates both with invasion and motility, and likely plays a direct role in promoting motility; that forced expression of E-cadherin in invasive, N-cadherin–positive cells does not reduce their motility or invasive capacity; that forced expression of N-cadherin in noninvasive, E-cadherin–positive cells produces an invasive cell, even though these cells continue to express high levels of E-cadherin; that N-cadherin–dependent motility may be mediated by FGF receptor signaling; and that cadherin-11 promotes epithelial cell motility in a manner similar to N-cadherin. |
format | Text |
id | pubmed-2151177 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 1999 |
publisher | The Rockefeller University Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-21511772008-05-01 N-Cadherin Promotes Motility in Human Breast Cancer Cells Regardless of Their E-Cadherin Expression Nieman, Marvin T. Prudoff, Ryan S. Johnson, Keith R. Wheelock, Margaret J. J Cell Biol Original Article E-cadherin is a transmembrane glycoprotein that mediates calcium-dependent, homotypic cell–cell adhesion and plays a role in maintaining the normal phenotype of epithelial cells. Decreased expression of E-cadherin has been correlated with increased invasiveness of breast cancer. In other systems, inappropriate expression of a nonepithelial cadherin, such as N-cadherin, by an epithelial cell has been shown to downregulate E-cadherin expression and to contribute to a scattered phenotype. In this study, we explored the possibility that expression of nonepithelial cadherins may be correlated with increased motility and invasion in breast cancer cells. We show that N-cadherin promotes motility and invasion; that decreased expression of E-cadherin does not necessarily correlate with motility or invasion; that N-cadherin expression correlates both with invasion and motility, and likely plays a direct role in promoting motility; that forced expression of E-cadherin in invasive, N-cadherin–positive cells does not reduce their motility or invasive capacity; that forced expression of N-cadherin in noninvasive, E-cadherin–positive cells produces an invasive cell, even though these cells continue to express high levels of E-cadherin; that N-cadherin–dependent motility may be mediated by FGF receptor signaling; and that cadherin-11 promotes epithelial cell motility in a manner similar to N-cadherin. The Rockefeller University Press 1999-11-01 /pmc/articles/PMC2151177/ /pubmed/10545506 Text en © 1999 The Rockefeller University Press This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/). |
spellingShingle | Original Article Nieman, Marvin T. Prudoff, Ryan S. Johnson, Keith R. Wheelock, Margaret J. N-Cadherin Promotes Motility in Human Breast Cancer Cells Regardless of Their E-Cadherin Expression |
title | N-Cadherin Promotes Motility in Human Breast Cancer Cells Regardless of Their E-Cadherin Expression |
title_full | N-Cadherin Promotes Motility in Human Breast Cancer Cells Regardless of Their E-Cadherin Expression |
title_fullStr | N-Cadherin Promotes Motility in Human Breast Cancer Cells Regardless of Their E-Cadherin Expression |
title_full_unstemmed | N-Cadherin Promotes Motility in Human Breast Cancer Cells Regardless of Their E-Cadherin Expression |
title_short | N-Cadherin Promotes Motility in Human Breast Cancer Cells Regardless of Their E-Cadherin Expression |
title_sort | n-cadherin promotes motility in human breast cancer cells regardless of their e-cadherin expression |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2151177/ https://www.ncbi.nlm.nih.gov/pubmed/10545506 |
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