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在骨髓瘤细胞系 (MG-63细胞) 中通过Quercetin-Doxorubicin组合抑制PI3K/Akt1通路

Mehmet Uğur Karabat¹, Mehmet Cudi Tuncer²

¹Department of Histology and Embryology, Medical Faculty, Dicle University, Diyarbakır 21280, Turkey.

Medicina (Kaunas, Lithuania)

|August 28, 2025

概括

奎尔塞丁 (Q) 和多克索鲁比辛 (Dox) 对骨肉瘤细胞具有协同作用. 结合Q和Dox可增强细胞亡,增加氧化应激,并抑制关键信号通路以改善治疗潜力.

科学领域:

癌症学
药理学
分子生物学

背景情况:

骨肉瘤 (OS) 是一种主要的骨癌,治疗选择有限.
奎尔塞丁 (Q) 是一种具有潜在抗癌性能的天然黄类化合物.
doxorubicin (Dox) 是一种常见的OS化疗剂.

研究的目的:

在MG-63骨肉瘤细胞系上研究奎尔塞丁和多克索鲁比辛的协同抗癌作用.
评估这种组合对细胞活力,细胞亡,氧化应激和关键信号通路的影响.

主要方法:

单独和组合使用奎尔塞丁和多克索鲁比辛治疗MG-63细胞.
评估了细胞活力 (MTT测定),细胞亡 (附录V/ PI,酶活性),活性氧物种 (ROS) 生成以及抗氧化酶水平.
使用RT-qPCR分析了Runx2,PI3K,Akt1和caspase-3的基因表达.

主要成果:

奎尔塞丁与多克索鲁比辛的结合显示出对MG-63细胞的协同毒性 (CI < 1).
联合治疗显著增强了细胞亡,增加了ROS水平,并降低了抗氧化酶活性.
基因表达分析显示caspase-3的上调和Runx2,PI3K和Akt1mRNA的下调.

结论:

在骨髓瘤细胞中表现出协同作用的抗癌活性.
这种组合诱导了亡,提高了氧化应激,抑制了抗氧化防御,并抑制了PI3K/ Akt1通路和Runx2表达.
奎尔塞丁可以作为有效的辅助剂来增强多克索鲁比辛在骨肉瘤治疗中的疗效.

关键词:

PI3K/Akt信号通道细胞亡骨质肉瘤扩散氨酸

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