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抑制RRM1可以使肺腺癌对德西他治疗敏感

Nan Jiang¹, Jianyong Liu², Ajay Vaghasia²

¹Department of Respiratory Disease, Thoracic Disease Center, The First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, China.

Cell death & disease

|February 26, 2026

概括

由于高的RRM1水平,肺癌细胞抵抗了德西他 (DAC). 抑制RRM1或核糖核酸减少酶 (RNR) 通过增加其DNA结合,增强瘤抑制基因活性和STING通路激活来提高DAC的疗效.

科学领域:

在瘤学瘤学.
分子生物学分子生物学
癌症基因组学癌症基因组学

背景情况:

异常的DNA甲基化对于肺癌的发展至关重要.
核酸模拟DNA甲基转移酶抑制剂在血液恶性瘤中表现有前途,但在固体瘤中有效性有限.
固体瘤中对这些药物产生初级耐药性的机制尚不清楚.

研究的目的:

调查RRM1在调解肺癌中对达西 (DAC) 内在耐药性的作用.
探索将DAC与RNR抑制剂结合用于增强肺癌治疗的潜力.

主要方法:

使用LC-MS/MS对RRM1表达率和DAC结合率的相关性分析.
通过RNA干扰介导的RRM1的耗尽和RNR的药理抑制.
评估肺癌细胞存活率,异种移植生长,瘤抑制基因重新激活和STING通路激活.
测量dCTP可用性和DAC纳入基因组DNA的测量.

主要成果:

RRM1表达与DAC整合相反相关.
抑制RRM1或RNR显著增强了DAC在体外和体内的抗癌作用.
通过降低dCTP水平,RRM1抑制增加了DAC的纳入.
联合治疗促进了瘤抑制基因的重新激活和STING通路的激活.

结论:

RRM1/RNR通路是肺癌中DAC抗性的关键决定因素.
DAC与RNR抑制剂的联合治疗是肺癌治疗的有前途的策略.
这种方法需要进一步的临床研究和翻译.

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