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阿特拉提洛西德抑制了耐基菲提尼布的非小细胞肺癌细胞的增殖

Wanxin Yao^1,2, Chen Liu³, Ningyin Zhang²

¹Affiliated Yongkang First People's Hospital and School of Pharmacy, Hangzhou Medical College, Hangzhou, Zhejiang 310014, P.R. China.

Oncology letters

|August 9, 2024

概括

传统中医药中的Atractyloside在治疗耐氨酸激酶抑制剂耐性非小细胞肺癌 (NSCLC) 中显示出潜力. 它模仿了抑制BORIS的效果,这是一种与NSCLC药物耐药性相关的蛋白质.

科学领域:

在瘤学瘤学.
分子生物学分子生物学
药理学药理学是指药理学的学科.

背景情况:

非小细胞肺癌 (NSCLC) 是一个重大的全球卫生挑战,死亡率高.
在NSCLC中复发通常是由表皮生长因子受体突变驱动的,使临床治疗复杂化,并需要新的治疗点.
印记部位调节器 (BORIS) 的兄弟,也称为CTCFL,与NSCLC的进展和耐化疗有关,包括西斯和多药耐药性.

研究的目的:

为了研究BORIS表达在耐氨酸激酶抑制剂 (TKI) 耐性NSCLC细胞中的作用.
评估向BORIS在TKI耐药NSCLC中的治疗潜力.
探索阿特拉提洛西德对NSCLC细胞的抗癌作用,特别是在TKI耐药性的背景下.

主要方法:

检查了TKI耐药NSCLC细胞系中的BORIS表达水平.
利用小干扰RNA (siRNA) 来击败BORIS表达,并评估其对细胞活性的影响.
采用MTT测试来确定atractyloside对NSCLC细胞增殖的影响.

主要成果:

分析了TKI抗性NSCLC细胞中的BORIS表达.
使用siRNA对BORIS的击败表明,它对抗TKI耐性NSCLC细胞的活力产生抑制作用.
发现,阿特拉提洛西德治疗抑制了抗TKI的NSCLC细胞的增殖,模仿了BORIS敲击的效果.

结论:

抑制BORIS或其下游途径为TKI耐药NSCLC提供了潜在的治疗策略.
通过调节与BORIS相关的途径,阿特拉提洛西德有效地抑制了对TKI耐药NSCLC细胞的增殖.
这些发现支持对阿特拉提洛西德作为TKI耐药NSCLC的治疗剂的研究.

关键词:

波里斯是不是一个好人?在NSCLCLC中,我们可以看到.具有TKI耐药性的技术亚特拉克提洛化物

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