Thus, antioxidants have the potential to treat brain injury and, thus, neuropsychiatric sequelae induced by blast exposure, such as memory loss and disorientation, under therapeutic conditions that also prevent pervasive sensorineural damage to the auditory system. Complementary performance evaluations, such as memory tests and spatial navigation, TH-302 should be conducted in the future to determine whether this treatment strategy can provide functional protection to brain injuries induced by blast exposure. Metastasis is a multi-step process that begins when tumor cells acquire the ability to degrade the basement membrane and move from the primary site of tumor formation to distant sites throughout the body, culminating in the formation of secondary tumors at these new sites. It is the formation of these secondary tumors that is the major cause of cancer-related deaths. In epithelial tissues, the abnormal proliferation, migration and invasion of constituent cells are limited by intercellular adhesive complexes, which tether neighboring cells to one another and maintain normal tissue architecture and function. The main adhesive complexes in epithelia are the cadherinbased adherens junction and desmosomes. Cadherins are single-pass transmembrane glycoproteins that make homotypic extracellular interactions with cadherin proteins on neighboring cells and intracellularly interact with catenin proteins. At the adherens junction, E-cadherin interacts with either b-catenin or ccatenin, which then interact with a-catenin, an actin binding protein, which tethers the cadherin-catenin complex to the actin cytoskeleton. Similarly, at the desmosome, the desmosomal cadherins are tethered to the intermediate filament cytoskeleton through interactions with plakoglobin and desmoplakin. b-catenin and plakoglobin are structural and functional homologs and 
members of the armadillo family of proteins with dual functions in cell-cell adhesion and cell signaling. Both proteins interact with E-cadherin, Axin and APC and both are involved in the Wnt signaling pathway through their interactions with the TCF/LEF transcription factors. Despite their structural similarities and common interacting partners, b-catenin and plakoglobin appear to have different signaling activities and regulate tumorigenesis in opposite manners. While b-cateninTCF/LEF complexes are transcriptionally active, several studies have demonstrated that plakoglobin-TCF complexes are inefficient in binding to DNA. Conversely, plakoglobin, but not b-catenin, interacts with p53 and regulates gene expression independent of TCF. Furthermore, b-catenin has welldocumented oncogenic signaling activities as the terminal component of the Wnt signaling pathway, whereas plakoglobin has typically been associated with tumor/metastasis suppressor activities. To determine the role of plakoglobin in tumorigenesis and metastasis, we previously expressed physiological levels of plakoglobin in the plakoglobin-null SCC9 cell line, a human squamous cell carcinoma cell line derived from the tongue. Plakoglobin expression in SCC9 cells resulted in a mesenchymal -to-epidermoid phenotypic transition that was concurrent with the Tubacin increased levels of Ncadherin, decreased levels of b-catenin and the formation of desmosomes. We subsequently performed proteomic and transcription microarray experiments to identify potential genes and proteins whose levels were differentially expressed following plakoglobin expression. These studies identified several tumor and metastasis suppressors and oncogenes whose levels were increased and decreased, respectively, in SCC9-PG cells. Among these differentially expressed genes was the global regulator of gene expression, Special AT-Rich Sequence Binding Protein 1. SATB1 was initially identified as a DNA-binding protein that was highly expressed in the thymus.