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Published 8 May 2006. doi:10.1083/jcb.200510087
The Rockefeller University Press, 0021-9525 $8.00
JCB, Volume 173, Number 3, 431-441
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Article

E-cadherin engagement stimulates proliferation via Rac1



Wendy F. Liu1,2, Celeste M. Nelson1, Dana M. Pirone2, and Christopher S. Chen2

1 Department of Biomedical Engineering, Johns Hopkins University School of Medicine, Baltimore, MD 21205
2 Department of Bioengineering, University of Pennsylvania, Philadelphia, PA 19104

Correspondence to Christopher S. Chen: chrischen{at}seas.upenn.edu

E-cadherin has been linked to the suppression of tumor growth and the inhibition of cell proliferation in culture. We observed that progressively decreasing the seeding density of normal rat kidney-52E (NRK-52E) or MCF-10A epithelial cells from confluence, indeed, released cells from growth arrest. Unexpectedly, a further decrease in seeding density so that cells were isolated from neighboring cells decreased proliferation. Experiments using microengineered substrates showed that E-cadherin engagement stimulated the peak in proliferation at intermediate seeding densities, and that the proliferation arrest at high densities did not involve E-cadherin, but rather resulted from a crowding-dependent decrease in cell spreading against the underlying substrate. Rac1 activity, which was induced by E-cadherin engagement specifically at intermediate seeding densities, was required for the cadherin-stimulated proliferation, and the control of Rac1 activation by E-cadherin was mediated by p120-catenin. Together, these findings demonstrate a stimulatory role for E-cadherin in proliferative regulation, and identify a simple mechanism by which cell–cell contact may trigger or inhibit epithelial cell proliferation in different settings.

Abbreviation used in this paper: NRK, normal rat kidney.


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