Tripartite motif 47 (TRIM47), a member of the TRIM protein family, plays a crucial role in tumor development and progression. However, the role of TRIM47 in glioma has not been investigated. In the present study, we investigated the expression of TRIM47 in glioma and explored the role of TRIM47 in glioma proliferation and migration both in vitro and in vivo. Our results showed that TRIM47 expression was significantly increased in glioma tissues compared to the normal brain tissues. Knockdown of TRIM47 in U87 and U251 cells inhibited cell proliferation, as well as cell migration and invasion. TRIM47 knockdown caused significant increase in E-cadherin expression and remarkable decrease in N-cadherin and vimentin expressions in both U87 and U251 cells. In vivo assay proved that knockdown of TRIM47 prevented tumor growth of glioma. Furthermore, TRIM47 silencing significantly inhibited the activation of Wnt/β-catenin pathway. Additionally, treatment with LiCl reversed the inhibitory effects of TRIM47 knockdown on cell proliferation and migration in U87 cells. In conclusion, these findings indicated that knockdown of TRIM47 suppressed cell proliferation and metastasis of glioma both in vitro and in vivo. TRIM47 exerted an oncogenic role in glioma and might be a therapeutic target for the treatment of glioma.

三方基序47（TRIM47）是TRIM蛋白家族的成员，在肿瘤的发生和发展中起着至关重要的作用。然而，尚未研究TRIM47在神经胶质瘤中的作用。在本研究中，我们调查TRIM47的表达在神经胶质瘤和探索TRIM47在两个神经胶质瘤的增殖和迁移的作用的体外和体内。我们的结果表明，与正常脑组织相比，胶质瘤组织中TRIM47的表达显着增加。敲除U87和U251细胞中的TRIM47可抑制细胞增殖以及细胞迁移和侵袭。TRIM47敲低导致U87和U251细胞中E-钙粘蛋白表达显着增加，N-钙粘蛋白和波形蛋白表达显着下降。体内分析证明，TRIM47的敲低阻止了神经胶质瘤的生长。此外，TRIM47沉默显着抑制Wnt /β-catenin途径的激活。另外，用LiCl处理逆转了TRIM47敲低对U87细胞中细胞增殖和迁移的抑制作用。总之，这些发现表明，在体外和体内，敲低TRIM47均可抑制胶质瘤的细胞增殖和转移。TRIM47在神经胶质瘤中发挥致癌作用，并且可能是治疗神经胶质瘤的治疗靶标。