Knocking down the expression of TRA2β inhibits the proliferation and migration of human glioma cells.

TRA2β 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 TRA2β is essential for normal mouse embryonic and brain development and has important roles in some cancers. However, the contribution of TRA2β 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 TRA2β in human glioma. To analyze the expression levels of TRA2β protein in glioma tissues, we performed immunohistochemical and Western blot analysis on human glioma tissues. The expression level of the TRA2β protein was significantly higher in high-grade gliomas than in low-grade gliomas. A strongly positive correlation was observed between TRA2β and Ki-67. More importantly, high expression of TRA2β was associated with a poor outcome. In vitro, after the release of U87 cell lines from serum starvation, the expression of TRA2β was upregulated, as well as PCNA and cyclin A. Knockdown of the TRA2β 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 TRA2β promotes glioma cell growth and migration, and could be a candidate for molecular targeting during gene therapy treatments of glioma.

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