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© The Rockefeller University Press, 0021-9525/1999//631 $5.00
The Journal of Cell Biology, Volume 147, Number 3, , 1999 631-644

Original Article

N-Cadherin Promotes Motility in Human Breast Cancer Cells Regardless of Their E-Cadherin Expression



Marvin T. Niemana, Ryan S. Prudoffa, Keith R. Johnsona, and Margaret J. Wheelocka

a Department of Biology, University of Toledo, Toledo, Ohio 43606
Department of Biology, University of Toledo, Toledo, OH 43606.(419) 530-7737(419) 530-1555

mwheelo{at}uoft02.utoledo.edu

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.

Key Words: N-cadherin • E-cadherin • breast cancer • motility • fibroblast growth factor receptor

© 1999 The Rockefeller University Press


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