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CD44/POU2F2/BCL9L轴通过MIF驱动的SPP1+TAM激活在结直肠癌转移中进行中介

Fan Zhang^1,2, Bingquan Zhao², Xueying Fan²

¹State Key Laboratory of Dampness Syndrome of Chinese Medicine, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, China.

International journal of biological sciences

|March 9, 2026

概括

表达SPP1的瘤相关巨细胞通过MIF/CD44/POU2F2/BCL9L轴驱动结直肠癌 (CRC) 转移. 针对这种途径提供了一个新的策略来抑制TAM激活和管理CRC.

科学领域:

免疫学免疫学免疫学
在瘤学瘤学.
分子生物学分子生物学

背景情况:

与瘤相关的巨细胞 (TAMs),特别是SPP1+ TAMs,与结直肠癌 (CRC) 预后不佳有关.
驱动这种关联的精确机制和潜在的治疗点在很大程度上是未知的.

研究的目的:

阐明SPP1+TAM和CRC细胞之间的相互作用机制.
确定关键的分子参与者和参与SPP1+TAMs介导的CRC转移的信号通路.

主要方法:

单细胞RNA测序 (scRNA-seq) 用于分析细胞相互作用.
在体外共同培养模型,体内肝转移模型.
临床组织微阵列分析 (n=42) 以验证发现.

主要成果:

迁移抑制因子 (MIF) 和其受体CD44被确定为SPP1+TAM和CRC细胞相互作用中的关键.
在体外和体外,MIF信号阻塞抑制了SPP1+TAM激活和CRC细胞诱导的血管生成.
在CRC患者中观察到高MIF表达和SPP1+TAM激活.
POU2F2和BCL9L被确定为MIF驱动激活途径中的关键转录因子.

结论:

MIF/CD44/POU2F2/BCL9L信号轴通过增强SPP1+TAMs的益血管性能力来促进CRC转移.
针对这一轴是抑制SPP1+TAM激活和管理CRC转移的有希望的治疗策略.

关键词:

多元期权基金和多元期权基金.在MIF/CD44/POU2F2/BCL9L信号轴上在POU2F2F2中.在SPP1+TAM中.结肠直肠癌转移的发生.

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