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通过在黑色素瘤微环境中的miR-150-3p代码传递,设计的纳米纤维平台同时触发了YAP依赖的铁灭,并重新编程了T细胞免疫力

Jiemin Wang¹, Zhenguo Zhao², Haopeng Yang¹

¹State Key Laboratory of Reproductive Regulation and Breeding of Grassland Livestock, School of Life Sciences, Inner Mongolia University, Hohhot 010020, Inner Mongolia, China.

|August 27, 2025

概括

工程外细胞囊 (EVs) 将miR-150-3p传递给黑色素瘤,诱导铁和增强免疫检查点阻塞 (ICB) 治疗. 这种基于RNA的新疗法克服了ICB的抗药性,

科学领域:

生物技术
癌症学
纳米医学

背景情况:

黑色素瘤是一种侵袭性癌症,治疗选择有限,并且经常对免疫检查点阻断 (ICB) 产生抵抗力.
细胞外囊泡 (EV) 对RNA疗法具有前景,但在载荷和瘤向方面面临挑战.
工程 EV 提供了一个潜在的解决方案, 以提高治疗效果和治疗黑色素瘤的有效性.

研究的目的:

在黑色素瘤中开发一个高效的miRNA包装和瘤特异向的EV策略.
在克服ICB耐药性方面研究工程EV (iEV-150) 的治疗潜力.
阐明iEV-150具有抗瘤作用和调节瘤微环境的机制.

主要方法:

通过共同表达miR-150-3p和Annexin A2 (ANXA2) 来创建工程EV (iEV-150),并使用iRGD进行表面修饰.
使用RNA测序,RIP,ChIP和露西法酶试验研究了机制.
在黑色素瘤模型中评估了ferroptosis诱导,治疗效果,生物分布和免疫调节.

主要成果:

ANXA2促进了miR- 150- 3p的选择性载入到EV中,iEV- 150显示了黑色素瘤细胞吸收和瘤积累的增强.
通过NF2-Hippo-YAP轴,iEV-150抑制了NF2,激活了YAP信号,并通过NF2-Hippo-YAP轴上调调节了ferroptosis基因 (ACSL4,CHAC1).
在黑色素瘤模型中,iEV-150促进了CD8+T细胞的透和激活,显著提高了ICB的疗效.

结论:

iEV-150集成了有效的miRNA加载,瘤向,铁灭诱导和免疫重编程.
这种设计的EV平台有效地克服了黑色素瘤的ICB抗性.
iEV-150代表了一种基于RNA的治疗策略,用于精确治疗黑色素瘤.

关键词:

细胞外囊泡铁症河马-YAP信号 miR-150-3p 的使用情况瘤微环境

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