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首页> 外文期刊>Central European Journal of Biology >Ropivacaine inhibits proliferation, migration, and invasion while inducing apoptosis of glioma cells by regulating the SNHG16/miR-424-5p axis
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Ropivacaine inhibits proliferation, migration, and invasion while inducing apoptosis of glioma cells by regulating the SNHG16/miR-424-5p axis

机译:Ropivacaine通过调节SNHG16 / miR-424-5P轴来抑制增殖,迁移和侵袭,同时诱导胶质瘤细胞的凋亡

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摘要

Background Regional anesthesia has anti-proliferative and pro-apoptotic effects in various cancers. Therefore, the purpose of this study was to investigate the effects of ropivacaine on the proliferation, migration, invasion, and apoptosis of glioma cells in vitro . Methods Under ropivacaine stimulation conditions, proliferation, apoptosis, migration, and invasion of glioma cells were determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2 H -tetrazol-3-ium bromide (MTT), flow cytometry, and transwell assays, respectively. Western blot assay was employed to measure the protein expression levels in glioma cells. The expression levels of small nucleolar RNA host gene 16 (SNHG16) and miR-424-5p were assessed by reverse transcription-quantitative polymerase chain reaction (RT-qPCR). The interaction relationship between SNHG16 and miR-424-5p was predicted and confirmed using a bioinformatics database and dual-luciferase reporter, RNA immunoprecipitation (RIP) and RNA pull-down assays. Results After treatment with ropivacaine, proliferation, migration, and invasion were repressed while apoptosis was enhanced in glioma cells in a dose-depended manner. In addition, ropivacaine impeded SNHG16 expression in glioma cells. Importantly, overexpression of SNHG16 abolished the ropivacaine-induced effects on glioma cells. Analogously, knockdown of miR-424-5p counteracted the function of ropivacaine in glioma cells. We also found that SNHG16 bound to miR-424-5p and negatively regulated miR-424-5p expression in glioma cells. The rescue experiments indicated that ropivacaine might regulate glioma progression by targeting the SNHG16/miR-424-5p axis. Conclusion Our findings revealed the anti-tumor effects of ropivacaine in glioma by targeting the SNHG16/miR-424-5p axis. These data might extend the understanding of regulatory mechanisms by which ropivacaine could suppress glioma development.
机译:背景技术区域麻醉在各种癌症中具有抗增殖和促凋亡作用。因此,本研究的目的是探讨Ropivaine对体外胶质瘤细胞增殖,迁移,侵袭和凋亡的影响。通过3-(4,5-二甲基噻唑-2-基)-2,5-二苯基-2h -Tetrazol-3-Ium溴( MTT),流式细胞术和Transwell测定。使用蛋白质印迹测定来测量胶质瘤细胞中的蛋白质表达水平。通过逆转录定量聚合酶链反应(RT-QPCR)评估小核仁RNA宿主基因16(SNHG16)和miR-424-5P的表达水平。使用生物信息组数据库和双荧光素酶报告,RNA免疫沉淀(RIP)和RNA下拉测定预测并确认了SNHG16和MIR-424-5P之间的相互作用关系。结果在用罗哌港治疗后,抑制了肾小血细胞以剂量依赖的方式在肾小血细胞中增强了抑制剂。此外,Ropivacaine阻碍了胶质瘤细胞中的SNHG16表达。重要的是,SNHG16的过表达废除了罗比卡因诱导对胶质瘤细胞的影响。类似地,miR-424-5p的敲低抵消了Ropivaine在胶质瘤细胞中的功能。我们还发现,SNHG16与miR-424-5p结合并对胶质瘤细胞中的miR-424-5p表达进行了负面调节。救援实验表明,Ropivacaine可以通过靶向SNHG16 / miR-424-5P轴来调节胶质瘤进展。结论我们的研究结果鉴于SNHG16 / miR-424-5P轴揭示了Ropivaine在胶质瘤中的抗肿瘤作用。这些数据可能会延长对罗比卡因可以抑制胶质瘤发展的监管机制的理解。

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