Knockdown of TRIM37 suppresses the proliferation, migration and invasion of glioma cells through the inactivation of PI3K/Akt signaling pathway

• Published in: Biomedicine & pharmacotherapy Vol. 99; pp. 59 - 64
• Main Authors: Tang, Shi-lei, Gao, Yuan-lin, Wen-zhong, Hu
• Format: Journal Article
• Language: English
• Published: France Elsevier Masson SAS 01.03.2018
• Subjects: Cell Line, Tumor; Cell Movement - genetics; Cell Proliferation - genetics; EMT; Gene Expression Regulation, Neoplastic; Gene Knockdown Techniques; Glioma; Glioma - genetics; Glioma - pathology; Humans; Invasion; Neoplasm Invasiveness; Nuclear Proteins - genetics; Nuclear Proteins - metabolism; Phosphatidylinositol 3-Kinases - metabolism; Proto-Oncogene Proteins c-akt - metabolism; Signal Transduction; TRIM37; TRIM37; Glioma; EMT; Invasion
• ISSN: 0753-3322; 1950-6007; 1950-6007
• DOI: 10.1016/j.biopha.2018.01.054

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.