Cell cycle protein suppression and p21 induction in differentiating caco2 cells. Evers, B. Mark, Tien C. Ko, Jing Li, E. Aubrey Thompson. Department of Surgery and Department of Human Biological Chemistry and Genetics, The University of Texas Medical Branch, Galveston, Texas 77555
APStracts 3:0145G, 1996.
Despite intensive efforts, the exact cellular mechanisms leading to gut differentiation and development remain largely undefined. The cyclins, the cyclin-dependent kinases (Cdks), and the Cdk inhibitors (e.g. p21 and p27) are proteins that are important for cell cycle progression, subsequent growth inhibition and differentiation of various cell types. The purpose of our study was to better define the role of these cell cycle proteins in gut differentiation using the CaCo2 human cell line which spontaneously differentiates to a small bowel phenotype, as demonstrated by induction of sucrase-isomaltase (SI) gene expression. We found that protein levels of the cyclins (both D-type and E) and the Cdks (both Cdk2 and 4) progressively decreased in postconfluent CaCo2 cells. Moreover, cyclin E-associated histone H1 kinase activity decreased in an analogous fashion as the cyclins and Cdks. In contrast, induction of the Cdk inhibitor p21 occurred by 3 days postconfluency which was prior to increases of SI mRNA levels. These changes in the cell cycle proteins which include a progressive decrease of the cyclins and Cdks and a concomitant induction of p21 suggest an important role for these proteins in CaCo2 cell differentiation. Identifying the cell cycle mechanisms responsible for intestinal cell differentiation will be important to our understanding of both normal gut development as well as gut neoplasia which involves aberrant regulation of cell cycle arrest.

Received 26 February 1996; accepted in final form 12 July 1996.
APS Manuscript Number G74-6.
Article publication pending Am. J. Physiol. (Gastrointest. Liver
Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 4 August 1996