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Published 17 September 2001. doi:10.1083/jcb.200104036
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© The Rockefeller University Press, 0021-9525/2001/9/1185 $5.00
The Journal of Cell Biology, Volume 154, Number 6, September 17, 2001 1185-1196

Article

E-cadherin regulates cell growth by modulating proliferation-dependent ß-catenin transcriptional activity



Andreas Stockinger1, Andreas Eger1, Julia Wolf1, Hartmut Beug2 and Roland Foisner1

1 Department of Biochemistry and Molecular Cell Biology, Vienna Biocenter, University of Vienna, A-1030 Vienna, Austria
2 Research Institute of Molecular Pathology, A-1030 Vienna, Austria

Address correspondence to Roland Foisner, Dept. of Biochemistry and Molecular Cell Biology, Biocenter, University of Vienna, Dr. Bohrgasse 9, A-1030 Vienna, Austria. Tel.: 43-1-4277-52856. Fax: 43-1-4277-52854. E-mail: foisner{at}abc.univie.ac.at

ß-Catenin is essential for E-cadherin–mediated cell adhesion in epithelial cells, but it also forms nuclear complexes with high mobility group transcription factors. Using a mouse mammary epithelial cell system, we have shown previously that conversion of epithelial cells to a fibroblastoid phenotype (epithelial-mesenchymal transition) involves downregulation of E-cadherin and upregulation of ß-catenin transcriptional activity. Here, we demonstrate that transient expression of exogenous E-cadherin in both epithelial and fibroblastoid cells arrested cell growth or caused apoptosis, depending on the cellular E-cadherin levels. By expressing E-cadherin subdomains, we show that the growth-suppressive effect of E-cadherin required the presence of its cytoplasmic ß-catenin interaction domain and/or correlated strictly with the ability to negatively interfere with ß-catenin transcriptional activity. Furthermore, coexpression of ß-catenin or lymphoid enhancer binding factor-1 or T cell factor 3 with E-cadherin rescued ß-catenin transcriptional activity and counteracted E-cadherin–mediated cell cycle arrest. Stable expression of E-cadherin in fibroblastoid cells decreased ß-catenin activity and reduced cell growth. Since proliferating cells had a higher ß-catenin activity than G1 phase–arrested or contact-inhibited cells, we conclude that ß-catenin transcriptional activity is essential for cell proliferation and can be controlled by E-cadherin in a cell adhesion-independent manner.

Key Words: carcinogenesis; catenins; cell proliferation; E-cadherin; LEF-1


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