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CD44v5增强IL-4/IL-4Rα/STAT6/SAM68 aix诱导M2极化,并促进三阴性乳腺癌的进展

Zhongjian Ji¹, Lan Wang¹, Xinyi Bao¹

¹Department of Clinical Laboratory, The Fourth Hospital of Harbin Medical University, Harbin, China.

Cancer biology & therapy

|November 30, 2025

概括

CD44v5通过增强M2巨分化,促进侵袭性三阴性乳腺癌 (TNBC). 向CD44v5提供了一种新的策略,用于为TNBC治疗重新编程瘤相关巨细胞 (TAMs).

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:

三阴性乳腺癌 (TNBC) 具有侵略性,治疗选择有限.
瘤相关巨细胞 (TAMs) 是TNBC进展的关键驱动因素.
了解TAM重编程机制对于开发新疗法至关重要.

研究的目的:

为了研究CD44v5在TAM极化中的作用.
探索CD44v5作为TNBC的治疗点.

主要方法:

使用单克隆抗体和淘汰细胞系评估CD44v5作用.
进行了细胞功能测试 (伤口愈合,入侵,殖民地形成).
测量了细胞因子分泌 (IL-4,IL-6) 和巨细胞极化标志物.

主要成果:

通过IL-4/IL-4R信号传递,M2巨细胞和TAMs促进TNBC.
CD44v5封锁抑制了M2极化,并促进了M1转移.
CD44v5与IL-4Rα结合在一起,防止其内部化.

结论:

CD44v5通过IL-4Rα/STAT6/IL-4通路促进M2极化,推动TNBC的进展.
CD44v5是重编程TAM和M2巨细胞的潜在治疗标.
向CD44v5为TNBC治疗提供了一种新的策略.

关键词:

在CD44v5中,CD44v5是什么?IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-4-IL-IL-4-IL-4-IL-4-IL-4-IL-IL-IL-IL-IL-IL-IL-IL-IL-IL-IL-IL-IL-IL-IL-IL-IL-IL-IL-IL-IL-IL-IL-IL-IL-IL-IL-IL-IL-IL-IL-IL-IL-IL-IL-IL-IL-IL is is is is is is is is is what you are is what you are 它们的IL-4Rα.瘤的免疫微环境与瘤相关的巨细胞.

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