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一个多维的奥米克框架确定了GPR35作为M2巨细胞激活的驱动因素,以及结直肠癌的不良预后

Shen Guan¹, Liangchen Zhu², Yue Tian³

¹Department of Colorectal Surgery, Clinical Oncology School of Fujian Medical University, Fujian Cancer Hospital, Fuzhou, China.

Frontiers in immunology

|March 6, 2026

概括

这项研究揭示了GPR35在结直肠癌 (CRC) 中驱动免疫逃避,阻碍了免疫治疗. 向GPR35可能会使冷瘤对治疗敏感,改善许多CRC患者的治疗结果.

科学领域:

在瘤学瘤学.
免疫学免疫学免疫学
基因组学就是基因组学.

背景情况:

结肠直肠癌 (CRC) 构成了重大的全球健康挑战,治疗成功往往取决于瘤微环境 (TME).
目前的免疫疗法只对一小部分患者有效,因此需要研究免疫逃避机制.

研究的目的:

构建一个完整的CRC TME单细胞地图.
确定CRC中免疫逃避和免疫治疗耐药性的关键调节者.

主要方法:

多队列单细胞RNA测序 (scRNA-seq) 数据的整合.
应用非负矩阵因子化 (NMF) 和加权基因共同表达网络分析 (WGCNA).
在四个独立的临床队列中验证发现.

主要成果:

鉴定了9个内异质元程序 (MPs),其中MP8与M2巨细胞激活相关.
GPR35被确定为MP8的主调节者,预测CRC患者的预后不佳.
高GPR35表达与免疫排除的TME相关,减少细胞毒性T细胞透,以及对免疫治疗的抵抗.

结论:

GPR35是一种新型的,癌细胞内在的驱动器,在CRC中导致免疫逃避和免疫疗法抵抗.
在"冷"的CRC瘤中,GPR35代表了一个潜在的治疗标,可以提高免疫治疗的疗效.

关键词:

在 GPR35 中使用.NMF (非负矩阵因子化) 是一种非负矩阵因子化.机器学习 (ML) 是指机器学习.在多个OMCIS.瘤微环境 (TME) 是指瘤微环境.

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