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压力通过改变中性粒细胞分化促进乳腺癌的肺转移

Pengfei Liu¹, Jie Zheng¹, Wenjing Ma¹

¹Medical Innovation Center, Shanghai East Hospital, Tongji University, School of Medicine and School of Life Sciences and Technology, Shanghai, China.

Cancer research

|September 24, 2025

概括

心理压力促进乳腺癌转移,通过诱导肺部的癌症应激性中性粒细胞 (CSP). 这些中性粒细胞招募癌细胞,增加肺转移. 针对这种压力中性粒细胞轴提供了新的治疗策略.

科学领域:

在瘤学瘤学.
免疫学免疫学免疫学
压力生理学压力生理学

背景情况:

心理压力是乳腺癌进展和预后不佳的已知危险因素.
压力影响乳腺癌转移的确切机制尚不完全理解.

研究的目的:

研究慢性压力在调节乳腺癌转移中的作用.
确定压力诱导转移的基础细胞和分子机制.

主要方法:

利用基因工程和移植的乳腺癌小鼠模型.
在肺前转移的微环境中进行单细胞RNA测序.
进行了伪实时轨迹分析,以追踪中性粒细胞分化.
研究了葡萄糖皮质体受体 (NR3C1) 和皮质的作用.
采用了中性粒细胞减少 (anti-Ly6G),基因淘汰 (CRISPR/Cas9) 和受体抑制 (BX471) 策略.

主要成果:

在老鼠模型中,慢性压力显著增加了乳腺癌瘤生长和肺转移.
在压力肺微环境中发现了一种新的癌症压力预制 (CSP) 中性粒细胞亚型,过度表达Ccl3,Ccl4,Cxcl2,Il1r2和Cebpb.
证明压力将中性粒细胞转移到CSP亚型,通过CCL3/CCL4介导的招募促进CCR1+乳腺癌细胞的肺转移.
表明向中性粒细胞,CCL3/CCL4或CCR1显著减少乳腺癌肺转移.

结论:

建立了一个压力-中性细胞-癌症轴,驱动乳腺癌肺转移.
通过葡萄皮糖类受体激活诱导的CSP中性粒细胞,在促进转移方面发挥着关键作用.
向癌细胞中的CSP中性粒细胞或CCR1通路,为预防或治疗乳腺癌转移提供了有前途的治疗策略.

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