Department of Neurosurgery, Huaihe Hospital of Henan University, Kaifeng 475000, Henan Province, China.
Department of Neurology, Kaifeng Central Hospital, Kaifeng 475000, Henan Province, China.
Biomed Pharmacother. 2018 Mar;99:59-64. doi: 10.1016/j.biopha.2018.01.054. Epub 2018 Jan 8.
Tripartite motif 37 (TRIM37), a member of the TRIM protein family, was involved in the tumorigenesis of several types of cancer. However, the expression pattern and role of TRIM37 in glioma remain unclear. Therefore, the aim of the present study was to investigate the role of TRIM37 in glioma, and to determine the molecular mechanisms. Our results demonstrated that TRIM37 was highly expressed in human glioma tissues and cell liens. Additionally, knockdown of TRIM37 dramatically inhibited the proliferation, migration/invasion, and the epithelial-mesenchymal transition (EMT) phenotype in glioma cells. Furthermore, knockdown of TRIM37 significantly reduced the levels of phosphorylated PI3K and Akt in U87MG cells, and an activator of PI3K/Akt signaling (SC79) partly reversed the inhibitory effects of si-TRIM37 on glioma cell proliferation and migration. Taken together, our results demonstrated that TRIM37 functions as an oncogene in the development and progression of glioma. TRIM37 knockdown inhibited the proliferation and invasion of human glioma cells at least in part through the inactivation of PI3K/Akt signaling pathway.
三结构域蛋白 37（TRIM37）是 TRIM 蛋白家族的一员，参与了多种类型癌症的肿瘤发生。然而，TRIM37 在神经胶质瘤中的表达模式和作用尚不清楚。因此，本研究旨在探讨 TRIM37 在神经胶质瘤中的作用及其分子机制。
我们的结果表明，TRIM37 在人神经胶质瘤组织和细胞系中高表达。此外，敲低 TRIM37 可显著抑制神经胶质瘤细胞的增殖、迁移/侵袭和上皮-间充质转化（EMT）表型。此外，敲低 TRIM37 可显著降低 U87MG 细胞中磷酸化 PI3K 和 Akt 的水平，而 PI3K/Akt 信号通路的激活剂（SC79）部分逆转了 si-TRIM37 对神经胶质瘤细胞增殖和迁移的抑制作用。
综上所述，我们的研究结果表明，TRIM37 在神经胶质瘤的发生和发展中起癌基因作用。TRIM37 敲低至少部分通过抑制 PI3K/Akt 信号通路的失活抑制人神经胶质瘤细胞的增殖和侵袭。
