QUICK SEARCH:   [advanced] Author: Keyword(s):
Home     Help     Feedback     Subscriptions     Archive     Search     Table of Contents

First published online September 19, 2007
doi: 10.1242/10.1242/jcs.03485

This Article Figures Only Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Aoki, K. Articles by Taketo, M. M. Search for Related Content PubMed PubMed Citation Articles by Aoki, K. Articles by Taketo, M. M. Social Bookmarking                         What's this?

Adenomatous polyposis coli (APC): a multi-functional tumor suppressor gene

Department of Pharmacology, Graduate School of Medicine, Kyoto University, Kyoto 606-8501, Japan

^* Author for correspondence (e-mail: taketo{at}mfour.med.kyoto-u.ac.jp)

Accepted 24 July 2007

The adenomatous polyposis coli (APC) gene is a key tumor suppressor gene. Mutations in the gene have been found not only in most colon cancers but also in some other cancers, such as those of the liver. The APC gene product is a 312 kDa protein that has multiple domains, through which it binds to various proteins, including -catenin, axin, CtBP, Asefs, IQGAP1, EB1 and microtubules. Studies using mutant mice and cultured cells have demonstrated that APC suppresses canonical Wnt signalling, which is essential for tumorigenesis, development and homeostasis of a variety of cell types, such as epithelial and lymphoid cells. Further studies have suggested that APC plays roles in several other fundamental cellular processes. These include cell adhesion and migration, organization of the actin and microtubule networks, spindle formation and chromosome segregation. Deregulation of these processes caused by mutations in APC is implicated in the initiation and expansion of colon cancer.

Key words: APC, Wnt signalling pathway, Colon cancer, Chromosome instability, Cell migration, Cell adhesion, -catenin, Asef, IQGAP1, Actin, EB1, Microtubules

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

This article has been cited by other articles:

				H. Beamish, L. de Boer, N. Giles, F. Stevens, V. Oakes, and B. Gabrielli Cyclin A/cdk2 Regulates Adenomatous Polyposis Coli-dependent Mitotic Spindle Anchoring J. Biol. Chem., October 16, 2009; 284(42): 29015 - 29023. [Abstract] [Full Text] [PDF]

				G. Martinez, M. Wijesinghe, K. Turner, H. E. Abud, M. M. Taketo, T. Noda, M. L. Robinson, and R. U. de Iongh Conditional Mutations of {beta}-Catenin and APC Reveal Roles for Canonical Wnt Signaling in Lens Differentiation Invest. Ophthalmol. Vis. Sci., October 1, 2009; 50(10): 4794 - 4806. [Abstract] [Full Text] [PDF]

				A. C. Kim, F. M. Barlaskar, J. H. Heaton, T. Else, V. R. Kelly, K. T. Krill, J. O. Scheys, D. P. Simon, A. Trovato, W.-H. Yang, et al. In Search of Adrenocortical Stem and Progenitor Cells Endocr. Rev., May 1, 2009; 30(3): 241 - 263. [Abstract] [Full Text] [PDF]

				B.J. Pearson and A. Sanchez Alvarado Regeneration, Stem Cells, and the Evolution of Tumor Suppression Cold Spring Harb Symp Quant Biol, January 15, 2009; (2009) sqb.2008.73.045v1. [Abstract] [PDF]

				T. Boutros, E. Chevet, and P. Metrakos Mitogen-Activated Protein (MAP) Kinase/MAP Kinase Phosphatase Regulation: Roles in Cell Growth, Death, and Cancer Pharmacol. Rev., September 1, 2008; 60(3): 261 - 310. [Abstract] [Full Text] [PDF]