Emerging roles of glycogen synthase kinase 3 in the treatment of brain tumors
- 1 Department of Radiation Oncology, Comprehensive Cancer Center, University of Alabama-Birmingham School of Medicine, Birmingham, AL, USA
- 2 Department of Cell Biology, University of Alabama-Birmingham, Birmingham, AL, USA
- 3 Department of Pharmacology and Toxicology, University of Alabama-Birmingham, Birmingham, AL, USA
The constitutively active protein glycogen synthase kinase 3 (GSK3), a serine/threonine kinase, acts paradoxically as a tumor suppressor in some cancers while potentiates growth in others. Deciphering what governs its actions is vital for understanding many pathological conditions, including brain cancer. What are seemingly disparate roles of GSK3 stems from the complex regulation of many cellular functions by GSK3. This review focuses on the regulation of GSK3, its role in survival, apoptosis and DNA damage, and finally its potential therapeutic impact in brain cancer. A thorough understanding of this versatile protein is critical for improving the outcome of various diseases, especially cancer.
Keywords: glycogen synthase kinase 3, neuroprotection, lithium, brain cancer, DNA damage, epidermal growth factor receptor, NFκB, apoptosis and autophagy
Citation: Mills CN, Nowsheen S, Bonner JA and Yang ES (2011) Emerging roles of glycogen synthase kinase 3 in the treatment of brain tumors. Front. Mol. Neurosci. 4:47. doi: 10.3389/fnmol.2011.00047
Received: 10 August 2011;
Accepted: 06 November 2011;
Published online: 25 November 2011.
Edited by:Jim Robert Woodgett, Mount Sinai Hospital, Canada
Reviewed by:Karl P. Giese, University of London, UK
Jim Robert Woodgett, Mount Sinai Hospital, Canada
Copyright: © 2011 Mills, Nowsheen, Bonner and Yang. This is an open-access article subject to a non-exclusive license between the authors and Frontiers Media SA, which permits use, distribution and reproduction in other forums, provided the original authors and source are credited and other Frontiers conditions are complied with.
*Correspondence: Eddy S. Yang, Department of Radiation Oncology, University of Alabama at Birmingham, 1700 6th Avenue South, 176F, HSROC Suite 2232, Birmingham, AL 35249-6832, USA. e-mail: firstname.lastname@example.org
†Caroline N. Mills and Somaira Nowsheen have contributed equally to this work.