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Physiol. Genomics (September 16, 2003). doi:10.1152/physiolgenomics.00078.2003
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Submitted on May 5, 2003
Accepted on September 11, 2003

Transcriptional Profiling of the Transition from Normal Intestinal Epithelia to Adenomas and Carcinomas in the APC(Min/+) Mouse

Nicholas F Paoni1*, Matthew W Feldman1, Linda S Gutierrez1, Victoria A Ploplis1, and Francis J Castellino1

1 Department of Chemistry and Biochemistry, University of Notre Dame, Notre Dame, IN, USA

* To whom correspondence should be addressed. E-mail: npaoni{at}nd.edu.

Mutations in the adenomatous polyposis coli (APC)3 gene that result in excessive {beta}-catenin-induced cell signaling are implicated in the risk of colon cancer. Although the mechanism of APC-mediated tumorigenesis is known, the pathways that translate {beta}-catenin signaling into tumor growth in vivo are undefined. To address this, gene expression profiles of normal intestinal epithelial cells were compared to those from adenomas and carcinomas from APC(Min/+) mice, a model of APC-related colorectal cancer. The gene expression profiles of adenomas and carcinomas were very similar, which is consistent with the theory that carcinomas progress from adenomas in this model system. Tumors had altered transcript abundance for members of several pathways that influence cell growth and proliferation including growth factors/receptors, molecules involved in apoptosis, and protein processing and catabolism enzymes. Comparison of gene expression between adenomas and carcinomas revealed 9 differentially expressed transcripts. These included members of 3 growth regulating pathways, and the results are consistent with the increased growth potential of carcinomas. SRY-box containing gene 17 (Sox 17), a negative regulator of {beta}-catenin signaling, and calbindin-D9K, a factor that enhances calcium transport, were more highly expressed in adenomas than carcinomas (approximately 4 and 15-22 fold, respectively). Transcript abundance for insulin-like growth factor binding protein-5, which mediates insulin-like growth factor function, was 2.6 fold greater in carcinomas. Because the changes in gene expression observed in this study are directly associated with a deficiency in APC, the data provide new insights into how loss of this important tumor suppressor translates into benign and malignant tumor growth.




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