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Oncogene. 2011 Sep 15;30(37):3979-84. doi: 10.1038/onc.2011.129. Epub 2011 May 2.

E2F1 suppresses Wnt/β-catenin activity through transactivation of β-catenin interacting protein ICAT.

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Department of Cancer Biology and Pharmacology, Genome Institute of Singapore, A*Star (Agency for Science, Technology and Research), Biopolis, Singapore.


Deregulation of the pRb/E2F or Wnt/β-catenin pathway occurs frequently in human cancers, which is often associated with inappropriate cell proliferation. Although the oncogenic roles of pRb/E2F1 and Wnt/β-catenin pathways have been well studied, the functional interaction between the two pathways has only recently been characterized. In particular, E2F1 has been recently reported to negatively regulate Wnt/β-catenin activity in human colorectal cancers, though the mechanism underlying this regulation is not fully understood. Here we provide evidence that β-catenin interacting protein 1 (CTNNBIP1), also known as ICAT (inhibitor of β-catenin and TCF4), functions as a crucial node to mediate the cross talk between E2F1 and β-catenin signaling. We show that ICAT is a direct transcriptional target of E2F1, and that activation of ICAT by E2F1 is required for E2F1 to inhibit β-catenin activity. This study provides a mechanistic insight into the antagonistic interaction between E2F1 and β-catenin signaling.

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