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Target genes of β-catenin–T cell-factor/lymphoid-enhancer-factor signaling in human colorectal carcinomas

Mann, B., Gelos, M., Siedow, A., Hanski, M. L., Gratchev, A., Ilyas, M., Bodmer, W. F., Moyer, M. P., Riecken, E. O., Buhr, H. J., Hanski, C.·1999·Proceedings of the National Academy of Sciences
DOI 10.1073/pnas.96.4.1603
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Abstract

Mutations in the adenomatous polyposis coli or β-catenin gene lead to cytosolic accumulation of β-catenin and, subsequently, to increased transcriptional activity of the β-catenin–T cell-factor/lymphoid-enhancer-factor complex. This process seems to play an essential role in the development of most colorectal carcinomas. To identify genes activated by β-catenin overexpression, we used colorectal cell lines for transfection with the β-catenin gene and searched for genes differentially expressed in the transfectants. There are four genes affected by β-catenin overexpression; three overexpressed genes code for two components of the AP-1 transcription complex, c -jun and fra-1 , and for the urokinase-type plasminogen activator receptor (uPAR), whose transcription is activated by AP-1. The direct interaction of the β-catenin–T cell-factor/lymphoid-enhancer-factor complex with the promoter region of c -jun and fra-1 was shown in a gel shift assay. The concomitant increase in β-catenin expression and the amount of uPAR was confirmed in primary colon carcinomas and their liver metastases at both the mRNA and the protein levels. High expression of β-catenin in transfectants, as well as in additionally analyzed colorectal cell lines, was associated with decreased expression of ZO-1, which is involved in epithelial polarization. Thus, accumulation of β-catenin indirectly affects the expression of uPAR in vitro and in vivo . Together with the other alterations, β-catenin accumulation may contribute to the development and progression of colon carcinoma both by dedifferentiation and through proteolytic activity.

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Metadata

Authors
Mann, B., Gelos, M., Siedow, A., Hanski, M. L., Gratchev, A., Ilyas, M., Bodmer, W. F., Moyer, M. P., Riecken, E. O., Buhr, H. J., & Hanski, C.
Affiliations
Departments of Surgery and Gastroenterology, Universitätsklinikum Benjamin Franklin, Freie Universität Berlin, 12200 Berlin, Germany; Cancer Genetics and Immunology Laboratory, Imperial Cancer Research Fund, Oxford OX3 9DU, United Kingdom; and InCell Corporation, San Antonio, TX 78258
Venue
Proceedings of the National Academy of Sciences
Publisher
National Academy of Sciences
Published
1999-02-16
Volume
96
Issue
4
Pages
1603-1608
ISSN
  • 0027-8424
  • 1091-6490
DOI
10.1073/pnas.96.4.1603
Cited by
663
References
0
Language
en

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