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Deguelin induces the apoptosis of lung cancer cells through regulating a ROS driven Akt pathway

机译:Deguelin通过调节ROS驱动的Akt途径诱导肺癌细胞凋亡

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Background Duguelin is a rotenoid extracted from plants and has potent antitumor effects in vitro and in vivo. However, the mechanism underlying the antitumor effect remains unclear. Our preliminary study showed that Deguelin is effective to stimulate the generation of Reactive Oxygen Species (ROS). In the current study, we evaluated the in vitro cytotoxicity of Deguelin against lung cancer cells and studied whether a ROS scavenger, N-acetyl-cysteine (NAC), can reverse the inhibitory effect of Deguelin. Results We showed that the dose-dependent apoptotic inducing effect of Deguelin could be partially reversed by the co-administration of NAC. Moreover, Deguelin reduced the phosphorylation of Akt protein and induced the apoptotic protein Caspase-3 in a dose-dependent manner. Co-treatment with NAC partially attenuated this effect and rescued some cells from apoptosis. Conclusion Deguelin induces the apoptosis of cancer cells through a ROS driven Akt pathway, which could translate into a promising therapeutic for lung cancer.
机译:背景Duguelin是从植物中提取的类胡萝卜素,在体外和体内均具有有效的抗肿瘤作用。但是,抗肿瘤作用的机制尚不清楚。我们的初步研究表明,Deguelin可有效刺激活性氧(ROS)的产生。在当前的研究中,我们评估了Deguelin对肺癌细胞的体外细胞毒性,并研究了ROS清除剂N-乙酰半胱氨酸(NAC)是否可以逆转Deguelin的抑制作用。结果我们发现,NAC的联合给药可以部分逆转Deguelin的剂量依赖性凋亡诱导作用。此外,Deguelin降低了Akt蛋白的磷酸化,并以剂量​​依赖的方式诱导了凋亡蛋白Caspase-3。与NAC共同处理可部分减弱这种作用,并从凋亡中拯救一些细胞。结论Deguelin通过ROS驱动的Akt途径诱导癌细胞凋亡,可能成为肺癌的一种有希望的治疗方法。

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