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首页> 外文期刊>CNS neuroscience & therapeutics. >microRNA cluster MC‐let‐7a‐1~let‐7d promotes autophagy and apoptosis of glioma cells by down‐regulating STAT3
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microRNA cluster MC‐let‐7a‐1~let‐7d promotes autophagy and apoptosis of glioma cells by down‐regulating STAT3

机译:MicroRNA Cluster MC-Let-7A-1〜Let-7D通过下调Stat3促进胶质瘤细胞的自噬和凋亡

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Background Accumulating evidence has highlighted the correlation between microRNAs (miRNAs) and the progression of glioma. However, the role of miR cluster MC‐let‐7a‐1?~?let‐7d in glioma remains elusive. Thus, the current study aimed to investigate the effect of miR cluster MC‐let‐7a‐1?~?let‐7d on glioma progression. Methods and Results Microarray data analysis provided data indicating the involvement of miR cluster MC‐let‐7a‐1?~?let‐7d in glioma via STAT3. The expression of let‐7a‐1, let‐7d, let‐7f‐1, and miR cluster MC‐let‐7a‐1?~?let‐7d was diminished in the glioma tissues and the cell lines. Additionally, our results revealed that STAT3 was a target gene of let‐7d, let‐7a‐1, and let‐7f‐1, which was further verified by the dual‐luciferase reporter gene assay. Moreover, STAT3 expression was negatively mediated by let‐7a‐1, let‐7d, and let‐7f‐1. Up‐regulated miR cluster MC‐let‐7a‐1?~?let‐7d or silenced STAT3 suppressed cell proliferation but accelerated cell apoptosis and autophagy. Moreover, restrained tumor growth was identified in the nude mice treated with miR cluster MC‐let‐7a‐1?~?let‐7d mimics or STAT3 siRNA. Conclusion Taken together, the miR cluster MC‐let‐7a‐1?~?let‐7d promotes glioma cell autophagy and apoptosis by repressing STAT3. The current study highlights the potential of the miR cluster MC‐let‐7a‐1?~?let‐7d as biomarkers and promising treatment strategies for glioma.
机译:背景技术累积证据突出了microRNAS(miRNA)与胶质瘤的进展之间的相关性。然而,MIR Cluster MC-Let-7A-1的作用?〜?Let-7D在胶质瘤中仍然难以捉摸。因此,目前的研究旨在探讨miR聚类mc-let-7a-1的影响吗?~~~ 7d对胶质瘤进展。方法和结果微阵列数据分析提供了数据,表明MiR集群MC-Let-7A-1的参与~~~~ 7D通过STAT3的胶质瘤。 Let-7A-1,Let-7D,Let-7F-1和MiR簇MC-Let-7a-1的表达式在胶质瘤组织和细胞系中减少了~~~ 7d。此外,我们的结果表明,STAT3是Let-7D,Let-7a-1和Let-7F-1的靶基因,其通过双荧光素酶报告基因测定进一步验证。此外,STAT3表达由Let-7A-1,Let-7D和Let-7F-1负介导。上调的miR簇mc-let-7a-1?〜α-7d或沉默的stat3抑制细胞增殖,但加速细胞凋亡和自噬。此外,在用miR簇mc-let-7a-1处理的裸鼠中鉴定受限制的肿瘤生长?~~~~~模拟或stat3 siRNA。结论组合在一起,MiR簇MC-Let-7A-1?~~ 7D通过压制STAT3来促进胶质瘤细胞自噬和细胞凋亡。目前的研究突出了MIR集群MC-Let-7A-1的潜力?〜?Let-7D作为生物标志物以及胶质瘤的有前途的治疗策略。

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