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[摘要]：Deregulation of the pRb/E2F or Wnt/beta-catenin pathway occurs frequently in human cancers, which is often associated with inappropriate cell proliferation. Although the oncogenic roles of pRb/E2F1 and Wnt/beta-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/beta-catenin activity in human colorectal cancers, though the mechanism underlying this regulation is not fully understood. Here we provide evidence that beta-catenin interacting protein 1 (CTNNBIP1), also known as ICAT (inhibitor of beta-catenin and TCF4), functions as a crucial node to mediate the cross talk between E2F1 and beta-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 beta-catenin activity. This study provides a mechanistic insight into the antagonistic interaction between E2F1 and beta-catenin signaling. Oncogene (2011) 30, 3979-3984; doi:10.1038/onc.2011.129; published online 2 May 2011 |
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