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首页> 外文期刊>Journal of Cancer >MRPS16 facilitates tumor progression via the PI3K/AKT/Snail signaling axis
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MRPS16 facilitates tumor progression via the PI3K/AKT/Snail signaling axis

机译:MRPS16通过PI3K / AKT /蜗牛信号轴促进肿瘤进展

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Background: Although aberrant expression of MRPS16 (mitochondrial ribosomal protein S16) contributes to biological dysfunction, especially mitochondrial translation defects, the status of MRPS16 and its correlation with prognosis in tumors, especially glioma, which is a common, morbid and frequently lethal malignancy, are still controversial. Methods: Herein, we used high-throughput sequencing to identify the target molecule MRPS16. Subsequently, we detected MRPS16 protein and mRNA expression levels in normal brain tissue (NBT) and different grades of glioma tissue. The molecular effects of MRPS16 in glioma cells were tested by Western blotting, quantitative polymerase chain reaction (qRT-PCR), EdU, CCK-8, colony formation, Transwell migration and invasion assays. Results: Intriguingly, we found that MRPS16 knockdown suppressed tumor cell growth, migration and invasion. Conversely, MRPS16 over-expression increased tumor cell growth, migration and invasion. In addition, subsequent mechanistic studies indicated that MRPS16 promoted glioma cell growth, migration and invasion by the activating PI3K/AKT/Snail axis. Furthermore, we observed that the decrease in tumor cell growth, migration, invasion and Snail expression mediated by MRPS16 knockdown could be rescued by Snail over-expression. Conclusion: In short, our data demonstrate that MRPS16 over-expression remarkably promotes tumor cell growth, migration and invasion via the PI3K/AKT/Snail axis, which may be a promising prognostic marker for glioma.? The author(s).
机译:背景:虽然MRPS16(线粒体核糖体蛋白S16)的异常表达有助于生物功能障碍,尤其是线粒体翻译缺陷,MRPS16的状态及其与肿瘤预后的相关性,尤其是胶质瘤,这是一种常见的,病态和常见的恶性肿瘤仍有争议。方法:在此,我们使用高通量测序来鉴定靶分子MRPS16。随后,我们在正常脑组织(NBT)和不同等级的胶质瘤组织中检测MRPS16蛋白和mRNA表达水平。通过Western印迹,定量聚合酶链反应(QRT-PCR),EDU,CCK-8,菌落形成,转发迁移和侵袭测定来测试MRPS16在胶质瘤细胞中的分子效应。结果:有趣的是,我们发现MRPS16敲毁抑制肿瘤细胞生长,迁移和侵袭。相反,MRPS16过表达增加肿瘤细胞生长,迁移和侵袭。此外,随后的机制研究表明MRPS16通过激活PI3K / AKT /蜗牛轴促进了胶质瘤细胞生长,迁移和侵袭。此外,我们观察到,MRPS16敲低介导的肿瘤细胞生长,迁移,侵袭和蜗牛表达的降低可以通过蜗牛过度表达来救出。结论:简而言之,我们的数据表明MRPS16过表达显着促进了通过PI3K / AKT /蜗牛轴的肿瘤细胞生长,迁移和侵袭,这可能是胶质瘤的有希望的预后标志物。作者。

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