Autor: |
Huiqing Li, Xiaobo Fu, Huiyu Guo, Yue Sun, Di Wang, Zengzhen Zhang |
Rok vydání: |
2022 |
Předmět: |
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Zdroj: |
Saudi medical journal. 43(11) |
ISSN: |
0379-5284 |
Popis: |
To determine whether sevoflurane regulates cisplatin resistance in neuroblastoma cells.The SH-SY5Y cell line with cisplatin-resistant phenotype (SH-SY5Y-SR) was generated. Cells were co-treated with sevoflurane and cisplatin to seek the sevoflurane function on cisplatin resistance. Key targets of sevoflurane treatment were determined using sequencing (ribonucleic acid [RNA-seq]). Cells were then transfected with specific vectors. Linc00473 and microRNA-490-5p (miR-490-5p) levels were detected using reverse transcriptase quantitative real-time reverse transcription PCR (RT-qPCR). Linc00473-miR-490-5p binding was confirmed using a luciferase reporter-gene assay. After treatment, cell proliferation, viability, and caspase-3 activity were measured to determine the effects of treatment on tumor cells. Each experimental result is based on three independent experiments.Co-treatment with sevoflurane and cisplatin markedly improved the sensitivity of SH-SY5Y-SR cells to cisplatin, which inhibited the occurrence of cisplatin resistance. The RNA-sequencing analysis and RT-qPCR showed that sevoflurane inhibited linc00473 expression. Overexpression of linc00473 promoted cell proliferation, inhibited apoptosis, and promoted cisplatin resistance. The linc00473/miR-490-5p/V-akt murine thymoma viral oncogene homolog 1 (AKT1) axis was found to mediate the regulatory effects of sevoflurane on cisplatin resistance.Sevoflurane has great clinical potential against cisplatin-resistant tumors. Further animal experiments and clinical trials are required to achieve this goal. |
Databáze: |
OpenAIRE |
Externí odkaz: |
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