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Knockdown of Aurora-B inhibits the growth of non-small cell lung cancer A549 cells

机译:敲低Aurora-B抑制非小细胞肺癌A549细胞的生长

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摘要

Elevated expression of Aurora-B affects cell apoptosis and proliferation in a variety of solid tumors. However, the role of Aurora-B has been poorly evaluated in non-small cell lung cancer (NSCLC). In the present study, it was found that Aurora-B was overexpressed in tissue specimens obtained from 174 patients with lung cancer. It was also demonstrated that knockdown of Aurora-B induces apoptosis and inhibits the growth of lung cancer A549 cells in vitro and in vivo. Furthermore, it was found that silencing Aurora-B decreased the activity of the phosphoinositide 3-kinase (PI3K)/AKT pathway. Therefore, it was concluded that knockdown of Aurora-B induces apoptosis and inhibits growth in NSCLC A549 cells, in addition to inhibiting the activity of the PI3K/AKT signaling pathway. Targeting Aurora-B may provide a novel target for lung cancer therapy.
机译:Aurora-B的表达升高会影响多种实体瘤中的细胞凋亡和增殖。但是,在非小细胞肺癌(NSCLC)中,极光B的作用尚未得到很好的评估。在本研究中,发现从174名肺癌患者获得的组织样本中Aurora-B过表达。还证明了敲低Aurora-B在体外和体内诱导细胞凋亡并抑制肺癌A549细胞的生长。此外,发现沉默Aurora-B降低了磷酸肌醇3-激酶(PI3K)/ AKT途径的活性。因此,可以得出结论,敲除Aurora-B除了抑制PI3K / AKT信号通路的活性外,还可以诱导NSCLC A549细胞凋亡并抑制其生长。靶向Aurora-B可能为肺癌治疗提供新的靶点。

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