来自亲炎性M1巨细胞的细胞外囊泡在黑色素瘤细胞中诱导炎症和侵入性表型
Kaisa Mäki-Mantila1, Einari A Niskanen2, Kirsi Kainulainen2
1Institute of Biomedicine, School of Medicine, University of Eastern Finland, Kuopio, Finland. kaisa.maki-mantila@uef.fi.
Cell communication and signaling : CCS
|December 3, 2025
概括
支持炎症的M1巨细胞外囊泡 (EVs) 重新编程黑色素瘤细胞,通过NF-κB信号和瘤相关炎症增加入侵. 这突显了黑色素瘤进展中的EV介导通信.
科学领域:
- 在瘤学瘤学.
- 细胞生物学 细胞生物学
- 免疫学 免疫学 免疫学
背景情况:
- 黑色素瘤的进展涉及瘤微环境 (TME) 中的细胞间通信.
- 细胞外囊泡 (EVs) 介导货物转移,影响TME动态.
- 巨细胞衍生的EV在黑色素瘤中起作用,其丰富程度与预后不佳有关.
研究的目的:
- 调查M1 (促炎性) 和M2 (免疫抑制性) 巨细胞衍生的EVs对黑色素瘤细胞的影响.
- 了解巨细胞和黑色素瘤细胞之间的EV介导相互作用.
主要方法:
- 从M0,M1和M2极化THP-1巨细胞中隔离EVs.
- 用EVs治疗黑色素瘤细胞 (MV3,COLO800) 的方法.
- 对基因表达 (RNA-seq,qPCR),细胞因子概况,细胞入侵和信号通路 (NF-κB) 的分析.
主要成果:
- 在MV3黑色素瘤细胞中,M1 EVs诱导了亲炎性表型,上调了CXCL8,IL-6和IL-1β.
- M1 EV诱导的炎症增强了黑色素瘤细胞的侵袭,这种侵袭被CXCL8沉默扭转.
- M1 EVs激活了NF-κB通路,驱动了与炎症相关的基因表达.
结论:
- 通过NF-κB信号传递,M1巨衍生的EVs通过NF-κB信号传递在黑色素瘤中促进与瘤相关的炎症.
- 通过EV介导的巨细胞与瘤细胞的通信对于黑色素瘤的进展至关重要.
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