Abstract
Expression levels of Transformer 2 protein homolog beta (TRA2B) in patients with endometrial carcinoma were assessed to investigate the impact of TRA2B on endometrial carcinoma cells. Furthermore, we analyzed the expression of several genes in the tissue samples from patients with endometrial cancer (EC) to identify whether cancer related genes we chose are differently expressed between the endometrial carcinoma tissues and adjacent normal tissues. The results of RT-qPCR analysis, western blot technology and immunofluorescence method consistently manifested that the expression of several genes in endometrial carcinoma tissue was significantly dysregulated between the two groups. Among the dysregulated genes, the strongly upregulated TRA2B in the tissues and serum from patients with EC was selected for further analysis. Endometrial carcinoma cells were transfected with chemically synthesized TRA2B plasmid, siRNA-TRA2B and their corresponding negative control respectively to assess the effects of TRA2B on the EC cells. Overexpression of TRA2B increased both the cell viability and proliferation potency of EC cells. Whereas, the viability and the proliferation ability of EC cells were strongly decreased by siRNA-TRA2B treatment. Furthermore, the invasion of EC cells was promoted by transfection of TRA2B and overexpression of TRA2B decreased the apoptosis of EC cells. Moreover, siRNA-TRA2B transfection inhibited the invasion but accelerated apoptosis of EC cells. Our results demonstrated that TRA2B is closely related to the development of endometrial carcinoma, and inhibition of TRA2B can decrease viability, proliferation and invasion of endometrial carcinoma, suggesting TRA2B is associated with the pathogenesis of human EC. Knockdown of TRA2B may be used for treatment of endometrial carcinoma, furthermore, these findings suggest an experimental foundation to clinical prognostic role of TRA2B in patients with endometrial carcinoma.