Japanese Journal of Clinical Oncology 32:358-362 (2002)
© 2002 Foundation for Promotion of Cancer Research
Mutation and Expression of the ß-Catenin-interacting Protein ICAT in Human Colorectal Tumors
1 Second Department of Surgery, Gunma University School of Medicine, Maebashi, 2 Laboratory of Molecular and Genetic Information, Institution of Molecular and Cellular Biosciences, The University of Tokyo, Tokyo and 3 Biology Division, National Cancer Center Research Institute, Tokyo, Japan
Background: Aberrant activation of Wnt signaling caused by mutations in the tumor suppressor adenomatous polyposis coli or ß-catenin is a critical event in the development of human colorectal tumors. We have recently identified the ICAT gene, which encodes a small protein that interacts with ß-catenin and represses Wnt signaling.
Methods: We examined the prevalence of mutations in the entire ICAT coding sequence and intronic splice donor and acceptor regions of ICAT by PCR–SSCP and also the expression of the ICAT gene by RT-PCR.
Results: The ICAT gene was mapped to chromosome 1p36.1–p36.2, which is implicated in the pathogenesis of various types of cancers. However, no mutations in ICAT were detected among 128 colorectal tumors. Instead, ICAT was found to be overexpressed in almost half of colorectal carcinomas. Cases exhibiting ICAT overexpression showed a significantly higher incidence of well-differentiated adenocarcinoma and positive lymphatic permeation.
Conclusion: Our results suggest that ICAT is not the putative tumor suppressor on 1p36.1–p36.2, although aberrant overexpression of ICAT may play a role in the pathogenesis of colorectal carcinomas.
+ For reprints and all correspondence: Tetsu Akiyama, Department of Molecular and Genetic Information, Institution for Molecular and Cellular Biosciences, The University of Tokyo, 1–1–1 Yayoi, Bunkyo-ku, Tokyo, Japan. E-mail: akiyama@imcbns.iam.u-tokyo.ac.jp
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