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来自瘤的RAB21+ABHD12+sEVs驱动肺部的前转移性微环境

Kun Wu^{1,2,3,4,5,6,7,8}, Yan Li^1,4, Yikang Ji^1,5,6,7,8

¹Department of Oral and Maxillofacial-Head and Neck Oncology, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.

Cancer immunology research

|January 12, 2024

概括

头部和部状细胞癌 (HNSCC) 细胞释放小细胞外囊泡 (sEVs),通过创建免疫抑制性转移前的利基,促进肺转移. 针对这些SEV可以提高抗PD-1疗法的疗效.

科学领域:

在瘤学瘤学.
免疫学免疫学免疫学
细胞生物学细胞生物学

背景情况:

瘤转移包括创造一个前转移的利基,通常以免疫抑制性巨细胞为特征.
头部和部状细胞癌 (HNSCC) 转移依赖于建立这个主要瘤扩散的利基.

研究的目的:

研究HNSCC衍生的小细胞外囊 (sEVs) 在前转移性位形成和肺转移中的作用.
通过确定sEVs促进免疫抑制瘤微环境的分子机制.
探索针对sEVs的治疗策略,以加强癌症免疫治疗.

主要方法:

来自HNSCC细胞的sEV的表征,专注于RAB21和ABHD12货物.
在体外和体内研究评估sEVs与肺巨细胞的相互作用.
对巨细胞两极分化,基因表达 (S1PR1) 和信号通路 (AKT-FoxO1) 的分析.
在临床前瘤模型中针对S1PR1和PD-1的组合治疗的评估.

主要成果:

携带RAB21的HNSCC衍生的sEV向肺巨细胞.
在肺转移性瘤和巨细胞内,ABHD12表达升高.
带有ABHD12的HNSCCsEV极化了巨细胞到一种免疫抑制的表型,促进了前转移性利基形成.
ABHD12通过AKT-FoxO1通路对S1PR1进行了上调,增强了免疫抑制.
对S1PR1和PD-1的联合向显著改善了抗瘤反应.

结论:

来自HNSCC细胞的RAB21+ABHD12+sEV驱动免疫抑制性前转移性的形成,促进肺转移.
这些sEVs代表了一个潜在的治疗目标,以克服抗PD-1治疗的耐药性.
针对S1PR1通路与PD-1阻断一起,为提高抗瘤疗效提供了一个有希望的策略.

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