Apc gene mutation is associated with a dominant-negative effect upon intestinal cell migration. Academic Article uri icon

Overview

abstract

  • Apc-associated intestinal tumor formation appears to require functional loss of both Apc alleles. Apc has, therefore, been classified as a tumor suppressor gene. Loss of APC protein function results in increased intracellular beta-catenin, a molecule important to both cell-cell adhesion and regulation of cellular growth. In mice bearing a germ-line Apc mutation, we found that enterocyte beta-catenin expression was also increased in histologically normal intestinal mucosa. Enterocyte crypt-villus migration was decreased by 25%, and treatment of Min/+ animals with sulindac sulfide normalized both beta-catenin expression and enterocyte migration. Our data suggest that alterations in enterocyte migration occur in cells bearing a single mutant Apc allele, and that sulindac sulfide may normalize enterocyte growth in these cells.

publication date

  • November 15, 1997

Research

keywords

  • Cell Movement
  • Cytoskeletal Proteins
  • Genes, APC
  • Intestine, Small
  • Trans-Activators

Identity

Scopus Document Identifier

  • 0030703623

PubMed ID

  • 9371501

Additional Document Info

volume

  • 57

issue

  • 22