TRIM31 enhances chemoresistance in glioblastoma through activation of the PI3K/Akt signaling pathway
| Autor: | Bing‑Yu Liu, Zhi‑Ping Dun, Chengwei Wang, Xue‑Ying Zhao, Ming‑De Fan, Yang Jiang, Qi Pang, Rui Zhang, Jian‑Ni Qi |
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| Rok vydání: | 2019 |
| Předmět: |
0301 basic medicine
Cancer Research 03 medical and health sciences 0302 clinical medicine Immunology and Microbiology (miscellaneous) Glioma medicine Viability assay Protein kinase B PI3K/AKT/mTOR pathway PI3K/Akt Temozolomide Akt/PKB signaling pathway Chemistry glioblastoma apoptosis chemoresistance Articles General Medicine tripartite motif-containing 31 Cell cycle medicine.disease 030104 developmental biology Apoptosis 030220 oncology & carcinogenesis Cancer research medicine.drug |
| Zdroj: | Experimental and Therapeutic Medicine |
| ISSN: | 1792-0981 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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