Making Cancer Quiescent: SPDEF De-Cycles Beta-Catenin Barbara Fingleton  Gastroenterology  Volume 153, Issue 1, Pages 10-12 (July 2017) DOI: 10.1053/j.gastro.2017.05.041 Copyright © 2017 Terms and Conditions

Figure 1 The paper from Lo et al suggests a provocative model whereby SPDEF can act as a ‘tipping point’ for β-catenin gene programs in transformed colonic epithelium. In the absence of SPDEF, β-catenin can interact with several of its partner transcription factors of the Lef/Tcf family, and transcription of both stem cell and cell cycle targets is possible. However, when SPDEF is present, its binding to the Arm repeats of the β-catenin protein prevents accessibility for a subset of Tcf family members (TCF-1 and -3) and only the stem cell program is engaged, with cells entering into quiescence in the absence of proliferative signals. This figure is simplified to emphasize the β-catenin interactions with Tcf family members and does not include the array of additional proteins that form β-catenin transcriptional complexes. Gastroenterology 2017 153, 10-12DOI: (10.1053/j.gastro.2017.05.041) Copyright © 2017 Terms and Conditions