2. Academic Validation
  3. TRIM31 enhances chemoresistance in glioblastoma through activation of the PI3K/Akt signaling pathway

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

  • Exp Ther Med. 2020 Aug;20(2):802-809. doi: 10.3892/etm.2020.8782.
Ming-De Fan 1 2,  Xue-Ying Zhao 3,  Jian-Ni Qi 4,  Yang Jiang 5,  Bing-Yu Liu 6,  Zhi-Ping Dun 1,  Rui Zhang 2,  Cheng-Wei Wang 1,  Qi Pang 2
Affiliations

Affiliations

  • 1 Department of Neurosurgery, The Second Hospital, Cheeloo College of Medicine, Shandong University, Jinan, Shandong 250033, P.R. China.
  • 2 Department of Neurosurgery, Shandong Provincial Hospital, Cheeloo College of Medicine, Shandong University, Jinan, Shandong 250021, P.R. China.
  • 3 Department of Transfusion, The Second Hospital, Cheeloo College of Medicine, Shandong University, Jinan, Shandong 250033, P.R. China.
  • 4 Central Laboratory, Shandong Provincial Hospital, Cheeloo College of Medicine, Shandong University, Jinan, Shandong 250021, P.R. China.
  • 5 Department of Hematology and Cellular Therapy, The Second Hospital, Cheeloo College of Medicine, Shandong University, Jinan, Shandong 250033, P.R. China.
  • 6 Department of Immunology, Key Laboratory of Infection and Immunity of Shandong Province, School of Biomedical Sciences, Cheeloo College of Medicine, Shandong University, Jinan, Shandong 250012, P.R. China.
PMID: 32765650 DOI: 10.3892/etm.2020.8782
Abstract

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 IC50 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.

Keywords

PI3K/Akt; apoptosis; chemoresistance; glioblastoma; tripartite motif-containing 31.

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