Knocking down the expression of TRA2 beta inhibits the proliferation and migration of human glioma cells

TRA2 beta protein is encoded by the TRA2B gene (also called SFRS10) on human chromosome 3. It functions as a sequence-specific serine/arginine splicing factor that plays a role in mRNA processing, splicing patterns, and gene expression. Previous studies have demonstrated that TRA2 beta is essential for normal mouse embryonic and brain development and has important roles in some cancers. However, the contribution of TRA2 beta gene dysfunction to the pathology of human diseases, such as gliomas, has not been addressed. This study aimed to assess the expression and function of TRA2 beta in human glioma. To analyze the expression levels of TRA2 beta protein in glioma tissues, we performed immunohistochemical and Western blot analysis on human glioma tissues. The expression level of the TRA2 beta protein was significantly higher in high-grade gliomas than in low-grade gliomas. A strongly positive correlation was observed between TRA2 beta and Ki-67. More importantly, high expression of TRA2 beta was associated with a poor outcome. In vitro, after the release of U87 cell lines from serum starvation, the expression of TRA2 beta was upregulated, as well as PCNA and cyclin A. Knockdown of the TRA2 beta gene resulted in suppression of the cell proliferation, cell cycle arrest during the G0/G1 phase, and a significant inhibition of cell migration. These results suggest that TRA2 beta promotes glioma cell growth and migration, and could be a candidate for molecular targeting during gene therapy treatments of glioma. (C) 2015 Elsevier GmbH. All rights reserved.