1. 14-3-3ζ Turns TGF-β to the Dark Side
Peter ten Dijke, Hans van Dam 
Cancer Cell 
Volume 27, Issue 2, Pages (February 2015)
DOI: /j.ccell
Copyright © 2015 Elsevier Inc. Terms and Conditions

2. Figure 1
14-3-3ζ Abrogates TGF-β/SMAD-Induced Growth Inhibition and Promotes Breast Cancer Metastasis
(A) ζ inhibits TGF-β/SMAD-induced growth inhibition by repressing YAP-induced σ expression. TGF-β receptor activation induces the formation of SMAD complexes, which can partner with p53 to activate p21 expression to inhibit cell cycle progression. p53 protein can be degraded by the E3 ubiquitin ligase MDM2, a process that is inhibited by σ. YAP is a transcriptional activator of σ. YAP can be sequestered in the cytoplasm by ζ and thereby interferes with σ expression.
(B) ζ promotes breast cancer metastasis by stabilizing GLI2. TGF-β-induced SMAD complexes interact with GLI2 to stimulate the expression of PTHrP. The E3 ligase βTrCP interacts with and mediates the degradation of GLI ζ can displace βTrCP from GLI2.
(C) Schematic representation of progressive stages in breast cancer. On the right side, relative levels of ζ, σ, YAP1, GLI2, phosphoSMAD2/3 (pSMAD2/3), p21, and PTHrP are indicated.
Cancer Cell  , DOI: ( /j.ccell )
Copyright © 2015 Elsevier Inc. Terms and Conditions