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Mutation and expression of the beta-catenin-interacting protein ICAT in human colorectal tumors
Toru Koyama1, Ken-Ichi Tago, Tsutomu Nakamura
1Second Department of Surgery, Gunma University School of Medicine, Maebashi, Laboratory of Molecular and Genetic Information, Institution of Molecular and Cellular Biosciences, The University of Tokyo, Tokyo, Japan.
Background:
Aberrant activation of Wnt signaling caused by mutations in the tumor suppressor adenomatous polyposis coli or beta-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 beta-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.
Insights
The ICAT gene, involved in Wnt signaling, showed no mutations in colorectal tumors. Instead, its overexpression correlated with well-differentiated adenocarcinoma and lymphatic permeation, suggesting a role in colorectal cancer progression.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Aberrant Wnt signaling, driven by APC or beta-catenin mutations, is key in colorectal tumor development.
- The ICAT gene encodes a protein that interacts with beta-catenin, repressing Wnt signaling.
Purpose of the Study:
- To investigate mutations and expression of the ICAT gene in colorectal tumors.
- To determine if ICAT acts as a tumor suppressor on chromosome 1p36.1-p36.2.
Main Methods:
- Mutation analysis of the entire ICAT coding sequence and splice regions using PCR-SSCP.
- Gene expression analysis of ICAT using RT-PCR in 128 colorectal tumors.
Main Results:
- No mutations in the ICAT gene were found in 128 colorectal tumors.
- ICAT was overexpressed in nearly half of colorectal carcinomas.
- ICAT overexpression was linked to well-differentiated adenocarcinoma and lymphatic permeation.
Conclusions:
- ICAT is unlikely to be the tumor suppressor gene on chromosome 1p36.1-p36.2.
- Aberrant overexpression of ICAT may contribute to colorectal carcinoma pathogenesis.
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