Please use this identifier to cite or link to this item: https://doi.org/10.1038/onc.2011.129
Title: E2F1 suppresses Wnt/Β-catenin activity through transactivation of Β-catenin interacting protein ICAT
Authors: Wu, Z.
Zheng, S.
Li, Z.
Tan, J.
Yu, Q. 
Keywords: cancer cells
E2F1
ICAT
Wnt/b-catenin
Issue Date: 15-Sep-2011
Citation: Wu, Z., Zheng, S., Li, Z., Tan, J., Yu, Q. (2011-09-15). E2F1 suppresses Wnt/Β-catenin activity through transactivation of Β-catenin interacting protein ICAT. Oncogene 30 (37) : 3979-3984. ScholarBank@NUS Repository. https://doi.org/10.1038/onc.2011.129
Abstract: 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. © 2011 Macmillan Publishers Limited All rights reserved.
Source Title: Oncogene
URI: http://scholarbank.nus.edu.sg/handle/10635/116989
ISSN: 09509232
DOI: 10.1038/onc.2011.129
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