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高CEBPB的休眠瘤细胞通过S100A8编排的瘤相关巨细胞重编程驱动免疫逃避

Jin Bai^1,2, Huilan Su³, Shunxi Wang^4,5

¹Department of Oncology, Shanghai East Hospital, Tongji University School of Medicine, 150 Jimo Road, Pudong District, Shanghai, 200120, China.

|March 9, 2026

概括

三阴性乳腺癌 (TNBC) 细胞通过保持休眠状态来逃避免疫治疗. 向CEPB-S100A8通路可以克服这种抵抗,并提高免疫检查点阻塞 (ICB) 治疗的有效性.

科学领域:

在瘤学瘤学.
免疫学免疫学免疫学
分子生物学分子生物学

背景情况:

三阴性乳腺癌 (TNBC) 对免疫检查点阻塞 (ICB) 的反应不佳.
休眠瘤细胞是免疫疗法耐药性和潜在瘤复发的重要储备.
在TNBC中瘤休眠和免疫逃避背后的机制需要进一步阐明.

研究的目的:

确定在接受ICB治疗的TNBC患者中维持瘤休眠的关键因素.
调查已识别的因素在免疫逃避中的作用及其作为治疗点的潜力.
阐明TNBC中瘤休眠,免疫抑制和ICB抵抗之间的分子机制.

主要方法:

利用公开的scRNA-seq数据来识别休眠的TNBC细胞.
采用了TetOn-H2BeGFP系统,用于体内和体外追踪休眠细胞.
执行CCK-8,殖民地形成,PI染色,流细胞计,IHC,多重免疫光学,RNA-seq和ChIP-seq以识别和验证CEPB的作用和下游目标.

主要成果:

休眠的TNBC细胞在免疫抑制利基 (M2巨细胞,低CD8+T细胞) 中被发现具有ICB耐药性.
鉴定出CEPBPB在休眠细胞中表达高,通过激活细胞循环抑制剂 (如CCNG2) 维持休眠状态.
通过巨细胞的招募和极化,CEPBPB促进了免疫抑制的微环境,S100A8被确定为M2极化的关键目标.

结论:

在TNBC中建立了瘤休眠和免疫逃避之间的机械联系.
突出了CEPB-S100A8轴作为免疫抑制和ICB抵抗的关键调解器.
证明向CEPB或S100A8可以克服ICB抵抗,并重塑瘤微环境以提高治疗效果.

关键词:

在CEBPBP的基础上,CEBPBP 休眠的瘤细胞是什么?在S100A8A8中使用.免疫检查点封锁封锁巨细胞是什么?巨细胞是什么?

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