| First Author | Mahmoud NN | Year | 1997 |
| Journal | Cancer Res | Volume | 57 |
| Issue | 22 | Pages | 5045-50 |
| PubMed ID | 9371501 | Mgi Jnum | J:44103 |
| Mgi Id | MGI:1099354 | Citation | Mahmoud NN, et al. (1997) Apc gene mutation is associated with a dominant-negative effect upon intestinal cell migration. Cancer Res 57(22):5045-50 |
| abstractText | 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. |
