SnoN signaling in proliferating cells and postmitotic neurons

The transcriptional regulator SnoN plays a fundamental role as a modulator of transforming growth factor beta (TGF beta)-induced signal transduction and biological responses. In recent years, novel functions of SnoN have been discovered in both TGF beta-dependent and TGF beta-independent settings in proliferating cells and postmitotic neurons. Accumulating evidence suggests that SnoN plays a dual role as a corepressor or coactivator of TGF beta-induced transcription. Accordingly, SnoN exerts oncogenic or tumor-suppressive effects in epithelial tissues. At the cellular level, SnoN antagonizes or mediates the ability of TGF beta to induce cell cycle arrest in a cell-type specific manner. SnoN also exerts key effects on epithelial-mesenchymal transition (EMT), with implications in cancer biology. Recent studies have expanded SnoN functions to postmitotic neurons, where SnoN orchestrates key aspects of neuronal development in the mammalian brain, from axon growth and branching to neuronal migration and positioning. In this review, we will highlight our understanding of SnoN biology at the crossroads of cancer biology and neurobiology. (C) 2012 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.