JCB logo
CrossRef
  Home | Help | Feedback | Subscriptions | Archive | Search | Table of Contents
Published 17 September 2001. doi:10.1083/jcb.200104036
This Article
Right arrow Full Text
Right arrow PDF (Full Text)
Right arrow Alert me when this article is cited
Right arrow Citation Map
Services
Right arrow Email this article
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new content in the JCB
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via CrossRef
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Stockinger, A.
Right arrow Articles by Foisner, R.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Stockinger, A.
Right arrow Articles by Foisner, R.
Social Bookmarking
Add to CiteULike   Add to Complore   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Reddit   Add to Technorati  
What's this?
© 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


Add to CiteULike CiteULike   Add to Complore Complore   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati    What's this?


This article has been cited by other articles:



  Home | Help | Feedback | Subscriptions | Archive | Search | Table of Contents