Reference SummaryPaoni NF, Physiol Genomics 2003 Nov 11;15(3):228-35


Transcriptional profiling of the transition from normal intestinal epithelia to adenomas and carcinomas in the APCMin/+ mouse.


Paoni NF; Feldman MW; Gutierrez LS; Ploplis VA; Castellino FJ


Physiol Genomics










Mutations in the adenomatous polyposis coli (APC) 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 with 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 nine differentially expressed transcripts. These included members of three 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-fold and 15- to 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.


J:86113 – MGI References
13130079 – National Library of Medicine/PubMed

Strain Notes

Strain Note
C57BL/6J These mice were from the Jackson Laboratory.
C57BL/6J-ApcMin/+ Mice were purchased from The Jackson Laboratory when 5 weeks old.


Strain Model Name Treatment Agent(s) Organ Affected Frequency Model Details
C57BL/6J-ApcMin/+ Intestine - Small Intestine - Ileum adenoma Intestine - Small Intestine - Ileum


C57BL/6J-ApcMin/+ Intestine - Small Intestine - Ileum carcinoma Intestine - Small Intestine - Ileum


C57BL/6J Intestine - Small Intestine - Ileum normal tissue (control) Intestine - Small Intestine - Ileum

not applicable