PMID:9371501

Citation	Mahmoud, NN, Boolbol, SK, Bilinski, RT, Martucci, C, Chadburn, A and Bertagnolli, MM (1997) Apc gene mutation is associated with a dominant-negative effect upon intestinal cell migration. Cancer Res. 57:5045-50
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.
Links	PubMed
Keywords	Analysis of Variance; Animals; Anti-Inflammatory Agents, Non-Steroidal/pharmacology; Apoptosis/drug effects; Cell Division/drug effects; Cell Division/genetics; Cell Movement/drug effects; Cell Movement/genetics; Cytoskeletal Proteins/metabolism; Female; Genes, APC/genetics; Intestinal Mucosa/cytology; Intestinal Mucosa/drug effects; Intestinal Mucosa/metabolism; Intestine, Small/cytology; Intestine, Small/drug effects; Intestine, Small/metabolism; Mice; Mice, Inbred C57BL; Proliferating Cell Nuclear Antigen/metabolism; Sulindac/pharmacology; Trans-Activators; beta Catenin
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