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M Sánchez-Ortega¹, A Garrido², C Cirauqui³

¹Department of Immunology and Oncology, National Centre for Biotechnology (CNB), Spanish Research Council (CSIC), Autonomous University of Madrid, Cantoblanco, Madrid, E-28049, Spain.

|August 13, 2024

概括

具有正常NFE2L2/KEAP1基因的肺状细胞癌 (LUSC) 对活性氧物种 (ROS) 敏感. ROS诱导通过特定的分子级联触发细胞死亡,这表明一种潜在的新型LUSC疗法.

科学领域:

在瘤学瘤学.
分子生物学分子生物学
癌症治疗方法癌症治疗方法

背景情况:

肺状细胞癌 (LUSC) 具有有限的可向驱动因素.
由KEAP1调节的NFE2L2 (NRF2) 途径在LUSC中经常活跃.
NRF2的激活可以保护人免受活性氧物种 (ROS) 的侵害,但其对LUSC对ROS敏感性的作用尚不清楚.

研究的目的:

调查LUSC具有正常NFE2L2/KEAP1基因对ROS敏感的假设.
阐明LUSC.中ROS诱导的细胞死亡背后的分子机制.
探索ROS诱导作为LUSC.治疗策略的潜力.

主要方法:

在LUSC瘤中分析NRF2激活.
在野生型NFE2L2/KEAP1 LUSC细胞中诱导ROS,并研究下游效应.
评估细胞死亡机制,包括铁亡,以及3D球体,有机体和异种移植中的分子通路 (miR-126,p85β,SETD5).

主要成果:

有活性NRF2的LUSC瘤受到ROS的保护,而野生型NFE2L2/KEAP1LUSC细胞经历了ROS诱导的铁亡.
ROS触发了一连串的过程,包括暂时的NRF2激活,miR-126上调,并降低了p85β和SETD5水平,导致毒性粉酶通路的激活.
同时耗尽p85β和SETD5诱导LUSC细胞死亡,而它们的过度表达挽救了细胞存活.

结论:

在正常NRF2LUSC中,NRF2 > miR-126 > p85β/SETD5级联介导ROS诱导的细胞死亡.
在各种LUSC模型中,暂时的ROS诱导有效地导致细胞死亡.
急性局部ROS诱导代表了LUSC患者正常NRF2.2的有前途的治疗策略.

关键词:

治疗LUSC的治疗方法我们的微RNA126 在PI3K中,PI3K是指PI3K.在SETD5中,我们使用了SETD5.暂时的ROS诱导剂暂时的ROS诱导剂 p85β ((PI3K) 的使用情况.

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