TRIM31 enhances chemoresistance in glioblastoma through activation of the PI3K/Akt signaling pathway

• Published in: Experimental and therapeutic medicine Vol. 20; no. 2; pp. 802 - 809
• Main Authors: Fan, Ming‑De, Zhao, Xue‑Ying, Qi, Jian‑Ni, Jiang, Yang, Liu, Bing‑Yu, Dun, Zhi‑Ping, Zhang, Rui, Wang, Cheng‑Wei, Pang, Qi
• Format: Journal Article
• Language: English
• Published: Athens Spandidos Publications 01.08.2020; Spandidos Publications UK Ltd; D.A. Spandidos
• Subjects: Antibodies; Apoptosis; Brain cancer; Cancer therapies; Care and treatment; Chemotherapy; Comparative analysis; Experiments; Glioblastomas; Glioma; Pancreatic cancer; Plasmids; Proteins; Radiation therapy; Software industry; Tumor proteins; Tumors; United States; China; Beijing China
• ISSN: 1792-0981; 1792-1015
• DOI: 10.3892/etm.2020.8782

Temozolomide (TMZ) resistance is a complication of treatment of glioma, and new strategies are urgently required to overcome chemoresistance in glioma cells. In the present study, it was demonstrated that tripartite motif-containing 31 (TRIM31) was abnormally upregulated in glioma tissues and cell lines compared with normal samples. Furthermore, the role of TRIM31 was assessed by overexpressing and knocking down its expression. Overexpression of TRIM31 increased cell viability, increased TMZ I[C.sub.50] values and inhibited apoptosis in A172 and U251 cells; whereas overexpression of TRIM31 decreased the expression of the apoptosis-associated protein p53. Knockdown of TRIM31 increased apoptosis in cells treated with TMZ. Additionally, the mechanisms by which TRIM31 affected glioma cells treated with TMZ were determined. Overexpression of TRIM31 increased phosphorylation of AKT and inhibiting the PI3K/AKT signaling pathway abolished the increase in cell viability and decreased phospho-Akt protein expression in TRIM31 overexpressing A172 cells treated with TMZ. Together, the findings suggest that TRIM31 may be a potentially novel target for glioma chemotherapy. Key words: glioblastoma, tripartite motif-containing 31, chemoresistance, PI3K/Akt, apoptosis