铜酸协调聚合物通过糖溶解重编程逆转非小细胞肺癌中的质死抵抗
Hui Liu1, Jianzhi Mao1, Mengxin Wang1
1The Education Ministry Key Lab of Resource Chemistry, Shanghai Municipal Education Committee Key Laboratory of Molecular Imaging Probes and Sensors, Shanghai Key Laboratory of Rare Earth Functional Materials, Shanghai Normal University, Shanghai 200234, China.
ACS nano
|January 1, 2026
概括
这项研究引入了一种新奇的纳米药物,可以通过重新编程瘤细胞代谢并增强铜诱导的毒性来克服非小细胞肺癌 (NSCLC) 对缩性 (铜诱导的细胞死亡) 的抵抗.
科学领域:
- 生物医学工程 生物医学工程
- 癌症治疗 癌症治疗
- 代谢重编程 代谢重编程
背景情况:
- 细胞亡是一种受调节的细胞死亡途径,是潜在的癌症治疗点.
- 非小细胞肺癌 (NSCLC) 由于高糖解活性而抵抗cuproptosis.
研究的目的:
- 开发一种超越NSCLC内在性cuproptosis耐药性的纳米平台.
- 调查代谢重编程和NSCLC中铜诱导毒性的协同效应.
主要方法:
- 一种协调聚合物 (Cu-Ox@HA) 在氨酸 (HA) 模板上用氧酸盐 (Ox) 结合铜离子的设计.
- 使用NSCLC模型 (A549异种移植) 的体外和体内研究.
- 评估 cuproptosis 的诱导,代谢途径的改变,以及治疗疗效.
主要成果:
- Cu-Ox@HA释放铜离子和Ox作为对谷氨 (GSH) 的反应,通过DLAT寡合化触发了cuproptosis.
- 氧沙酸抑制乳酸脱酶A,将瘤细胞代谢从糖解转移到氧化酸化.
- 证明了瘤生长抑制和体内延长生存时间,证实了治疗潜力.
结论:
- 开发的纳米平台通过代谢重编程和铜协同作用,有效地逆转NSCLC中的cuproptosis抵抗.
- 该策略通过准代谢脆弱性,为NSCLC治疗提供了一个有前途的方法.
- 提供了通过代谢-铜相互作用克服药物耐药性的机制性见解.
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