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  • Title: Should I stay or should I go: beta-catenin decides under stress.
    Author: Hoogeboom D, Burgering BM.
    Journal: Biochim Biophys Acta; 2009 Dec; 1796(2):63-74. PubMed ID: 19268509.
    Abstract:
    Reactive oxygen species (ROS) are essential for efficient and proper execution of a large number of cellular processes including signalling induced by exogenous factors. However, ROS are highly reactive in nature and excessive or prolonged ROS formation can result in considerable damage to cellular constituents and is implicated in the onset of a large variety of diseases as well as in the process of ageing [reviewed in [1] T.M. Paravicini, R.M. Touyz, Redox signaling in hypertension, Cardiovasc. Res. 71 (2006) 247-258, [2] P. Chiarugi, From anchorage dependent proliferation to survival: lessons from redox signalling, IUBMB life 60 (2008) 301-307, [3] M. Valko, D. Leibfritz, J. Moncol, M.T. Cronin, M. Mazur, J. Telser, Free radicals and antioxidants in normal physiological functions and human disease, Int. J. Biochem. Cell Biol. 39 (2007) 44-84]. Management of ROS to prevent potential damage, yet enabling its signalling function is achieved through numerous enzyme systems e.g. peroxidases, superoxide dismutases etc. and small molecules e.g. glutathione that collectively form the cellular anti-oxidant system. The O-class of Forkhead box (FOXO) transcription factors regulates amongst others cellular resistance against oxidative stress [[4] Y. Honda, S. Honda, The daf-2 gene network for longevity regulates oxidative stress resistance and Mn-superoxide dismutase gene expression in Caenorhabditis elegans, Faseb J. 13 (1999) 1385-1393]. In turn FOXOs themselves are regulated by ROS and cellular oxidative stress results in the activation of FOXOs [[5] M.A. Essers, S. Weijzen, A.M. de Vries-Smits, I. Saarloos, N.D. de Ruiter, J.L. Bos, B.M. Burgering, FOXO transcription factor activation by oxidative stress mediated by the small GTPase Ral and JNK, EMBO J. 23 (2004) 4802-4812]. A prominent feature of ROS-induced FOXO activation is ROS-induced binding of beta-catenin to FOXO [[6] M.A. Essers, L.M. de Vries-Smits, N. Barker, P.E. Polderman, B.M. Burgering, H.C. Korswagen, Functional interaction between beta-catenin and FOXO in oxidative stress signaling, Science (New York, NY) 308 (2005) 1181-1184, [7] M. Almeida, L. Han, M. Martin-Millan, C.A. O'Brien, S.C. Manolagas, Oxidative stress antagonizes Wnt signaling in osteoblast precursors by diverting beta-catenin from T cell factor- to forkhead box O-mediated transcription, J. Biol. Chem. 282 (2007) 27298-27305, [8] D. Hoogeboom, M.A. Essers, P.E. Polderman, E. Voets, L.M. Smits, B.M. Burgering, Interaction of FOXO with beta-catenin inhibits beta-catenin/T cell factor activity, J. Biol. Chem. 283 (2008) 9224-9230]. However, ROS affect many transcriptional programs besides that of FOXOs. Here, we discuss the recent progress in our understanding as to how ROS may regulate the interplay between some of the ROS-sensitive transcription factors through diverting beta-catenin binding to these transcription factors. We propose that beta-catenin acts as a key switch between the various ROS-sensitive transcription programs.
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