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通过SQSTM1/p62介导的PD-L1生物分子凝聚物形成促进了肺部瘤发生

Yen-Cheng Lin¹, Yu-Wei Lin¹, Rou-Hsin Wang²

¹Department of Biological Science and Technology, National Yang Ming Chiao Tung University, Hsinchu 300193, Taiwan.

Journal of advanced research

|February 23, 2026

概括

顺序素-1 (SQSTM1) 通过与编程死亡配体1 (PD-L1) 形成凝聚物,防止PD-L1降解,推动肺癌的进展. 针对这种相互作用为肺癌提供了潜在的治疗策略.

科学领域:

细胞生物学细胞生物学
癌症生物学癌症生物学
分子瘤学分子瘤学

背景情况:

生物分子凝结物对细胞功能至关重要,并与癌症有关.
顺序素-1 (SQSTM1) / p62是生物分子凝聚物形成的关键调节者.
编程死亡配体1 (PD-L1) 对于癌细胞生长和免疫规避至关重要.

研究的目的:

研究SQSTM1在调解PD-L1凝结物形成中的作用.
确定SQSTM1/PD-L1凝结物对肺瘤发生的贡献.
探索针对SQSTM1/PD-L1相互作用的治疗潜力.

主要方法:

免疫沉和免疫光,以评估SQSTM1-PD-L1相互作用和同位化.
截断的SQSTM1构造和AlphaFold3分析以确定交互的域.
使用1,6-hexanediol,Atezolizumab治疗和CRISPR/Cas9介导的SQSTM1淘汰对凝结物的破坏.
在体外,体内和临床相关性分析.

主要成果:

SQSTM1通过其PB1域直接与PD-L1相互作用,形成生物分子凝聚物.
这些凝结物防止PD-L1通过ubiquitin-proteasome系统降解,稳定PD-L1水平.
干扰SQSTM1/PD-L1凝聚物导致PD-L1降解,细胞活力降低,瘤生长减弱.
高SQSTM1和PD-L1表达与肺癌患者的预后不佳相关.

结论:

SQSTM1直接驱动非膜结合的PD-L1凝聚物的形成,稳定PD-L1并促进肺瘤发生.
SQSTM1/PD-L1凝结物通路代表了肺癌治疗的新型治疗标.

关键词:

生物分子凝聚剂是一种生物分子凝聚剂.PB1 域名 PB1 域名在PD-L1中.这就是SQSTM1的特点.瘤发生的起源

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