JCB logo
amgmicro.com
  Home | Help | Feedback | Subscriptions | Archive | Search | Table of Contents

Published 29 April 2002. doi:10.1083/jcb1573iti3
This Article
Right arrow Full Text (PDF, 565K)
Right arrow PPT slides of all figures
Right arrow Alert me when this article is cited
Services
Right arrow Email this article
Right arrow Similar articles in this journal
Right arrow Alert me to new content in the JCB
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via CrossRef
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Wells, W. A.
Right arrow Search for Related Content
PubMed
Right arrow Articles by Wells, W. A.
Related Collections
Right arrowRelated Article
Social Bookmarking
 Add to CiteULike   Add to Complore   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Facebook   Add to Reddit   Add to Technorati   Add to Twitter  
What's this?

© The Rockefeller University Press, 0021-9525/2002/4/344-a $5.00
The Journal of Cell Biology, Volume 157, Number 3, April 29, 2002 344-a-345


In This Issue

Wnt defeats death


Myc (arrow, top), but not Myc plus Wnt-1 (bottom) induces apoptosis in tumors.

To be successful, a tumorigenic cell must not only multiply but also fail to die. You et al. report that Wnt-1 contributes to both sides of this equation. Wnt-1 cooperates with Myc in promoting cell division, and blocks Myc's propensity to cause apoptotic cell death (page 429).

As a tumor promoter, Myc's apoptosis-promoting properties were paradoxical. Now, You et al. find that autocrine or paracrine coexpression of Wnt-1 with Myc prevents this apoptosis. Two Wnt-1 targets—WISP-1 and the cyclooxygenase Cox2—were induced in these cells. They can act together, and independently of Wnt-1, to reduce apoptosis sharply.Cells expressing Myc alone formed small tumors with many apoptotic cells, whereas cells coexpressing Myc and Wnt-1 formed large tumors. This may explain the coincidence of mutations in the Myc and Wnt pathways in many human tumors. Early loss of control over the Wnt pathway may both promote cell growth and inhibit apoptosis, with later mutations in proteins such as Myc accelerating the growth process. {blacksquare}



William A. Wells

wellsw{at}rockefeller.edu


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 Facebook Facebook   Add to Reddit Reddit   Add to Technorati Technorati   Add to Twitter Twitter    What's this?

Related Article

Wnt signaling promotes oncogenic transformation by inhibiting c-Myc–induced apoptosis
Zongbing You, Daniel Saims, Shaoqiong Chen, Zhaocheng Zhang, Denis C. Guttridge, Kun-liang Guan, Ormond A. MacDougald, Anthony M.C. Brown, Gerard Evan, Jan Kitajewski, and Cun-Yu Wang
J. Cell Biol. 2002 157: 429-440. [Abstract] [Full Text] [PDF]




This Article
Right arrow Full Text (PDF, 565K)
Right arrow PPT slides of all figures
Right arrow Alert me when this article is cited
Services
Right arrow Email this article
Right arrow Similar articles in this journal
Right arrow Alert me to new content in the JCB
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via CrossRef
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Wells, W. A.
Right arrow Search for Related Content
PubMed
Right arrow Articles by Wells, W. A.
Related Collections
Right arrowRelated Article
Social Bookmarking
 Add to CiteULike   Add to Complore   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Facebook   Add to Reddit   Add to Technorati   Add to Twitter  
What's this?


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