R-cadherin influences cell motility via Rho family GTPases
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Updated: Aug 24, 2026

RhoC GTPase Activation Assay
Published on: August 22, 2010
Emhonta Johnson1, Christopher S Theisen, Keith R Johnson
1Department of Oral Biology, College of Dentistry, Eppley Institute for Research in Cancer and Allied Diseases, and Eppley Cancer Center, University of Nebraska Medical Center, Omaha, Nebraska 68198, USA.
Abstract:
Classical cadherins are the transmembrane proteins of the adherens junction and mediate cell-cell adhesion via homotypic interactions in the extracellular space. In addition, they mediate connections to the cytoskeleton by means of their association with catenins. Decreased cadherin-mediated adhesion has been implicated as an important component of tumorigenesis. Cadherin switching is central to the epithelial to mesenchymal transitions that drive normal developmental processes. Cadherin switching has also been implicated in tumorigenesis, particularly in metastasis. Recently, cadherins have been shown to be engaged in cellular activities other than adhesion, including motility, invasion, and signaling. In this study, we show that inappropriate expression of R-cadherin in tumor cells results in decreased expression of endogenous cadherins (cadherin switching) and sustained signaling through Rho GTPases. In addition, we show that R-cadherin induces cell motility when expressed in epithelial cells and that this increased motility is dependent upon Rho GTPase activity.
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