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在AML HL-60细胞中,Z-ligustilide通过激活核受体NUR77和NOR1来首选引起线粒体功能障碍

Gen Liu¹, Zhi-Gang Chen¹, Li-Rong Yang¹

¹College of Pharmaceutical Sciences, College of Chinese Medicine, Southwest University, 2 Tiansheng Road, Beibei District, Chongqing, 400715, China.

Chinese medicine

|September 22, 2023

概括

Z-ligustilide (Z-LIG) 通过恢复NUR77和NOR1,诱导线粒体功能障碍和抑制mtDNA转录来选择性地向急性髓性白血病 (AML). 这为AML提供了一个新的治疗策略.

科学领域:

生物化学生物化学
分子生物学分子生物学
癌症研究癌症研究

背景情况:

核受体NUR77和NOR1是急性髓性白血病 (AML) 治疗的关键标.
通过调节NUR77和NOR1.1,Z-ligustilide (Z-LIG) 已经证明了对AML的选择性向.
在AML中Z-LIG的精确下游机制尚未完全阐明.

研究的目的:

调查Z-ligustilide (Z-LIG) 发挥其抗AML作用的下游机制.
阐明NUR77和NOR1在AML中Z-LIG介导的线粒体功能障碍中的作用.
探索Z-LIG作为AML治疗剂的潜力.

主要方法:

通过SRB染色来评估细胞活力.
通过流细胞计分析的亡,线粒体膜潜力和反应性氧物种.
用于识别Z-LIG标的RNA测序和定量RT-qPCR; 西方斑点证实了蛋白质表达.

主要成果:

在AML HL-60细胞中,Z-LIG优先诱导线粒体功能障碍.
RNA测序确定了线粒体转录和翻译作为潜在的Z-LIG标.
通过Z-LIG恢复NUR77/NOR1减少了线粒体ATP和膜潜力,增加了ROS,并抑制了线粒体转录/翻译,在体外和体内表现出抗AML活性.

结论:

通过NUR77/NOR1恢复,Z-LIG可以选择性地诱导AML细胞中的线粒体功能障碍.
这种机制涉及对线粒体DNA转录的干扰.
这些发现支持Z-LIG作为针对线粒体通路的AML有前途的治疗剂.

关键词:

急性骨髓性白血病 (AML) 是一种急性骨髓性白血病.线粒体功能障碍线粒体功能障碍没有NOR1 没有NOR1 在 NUR7777 中.这就是Z-ligustilide.

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