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Proc Natl Acad Sci U S A. 1999 Apr 27;96(9):4947-52.

T cell factor-activated transcription is not sufficient to induce anchorage-independent growth of epithelial cells expressing mutant beta-catenin.

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  • 1Department of Molecular and Cellular Physiology, Stanford University School of Medicine, Stanford, CA 94305-5345, USA. angelab@leland.stanford.edu

Abstract

N-terminal mutations in beta-catenin that inhibit beta-catenin degradation are found in primary tumors and cancer cell lines, and increased beta-catenin/T cell factor (TCF)-activated transcription in these cells has been correlated with cancer formation. However, the role of mutant beta-catenin in cell transformation is poorly understood. Here, we compare the ability of different N-terminal mutations of beta-catenin (DeltaN131, DeltaN90, DeltaGSK) to induce TCF-activated transcription and anchorage-independent growth in Madin-Darby canine kidney epithelial cells. Expression of DeltaN90 or DeltaGSK beta-catenin increased TCF-activated transcription but did not induce significant anchorage-independent cell growth. In contrast, deletion of the alpha-catenin-binding site in DeltaN131 beta-catenin reduced TCF-activated transcription, compared with that induced by DeltaN90 or DeltaGSK beta-catenin, but significantly enhanced anchorage-independent cell growth.

PMID:
10220399
[PubMed - indexed for MEDLINE]
PMCID:
PMC21797
Free PMC Article
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