通过TGF-β1介导的细胞间信号传输燃料合作性细胞入侵
Tala O Khatib1, Brian A Pedro2, Sergei Bombin3
1Department of Hematology and Medical Oncology, Emory University School of Medicine, Atlanta, GA 30322, USA; Winship Cancer Institute of Emory University, Atlanta, GA 30322, USA; Graduate Program in Biochemistry, Cell, and Developmental Biology, Emory University, Atlanta, GA 30322, USA.
Cell reports
|February 16, 2025
概括
癌细胞相互沟通,推动瘤生长和扩散. 这项研究表明,非小细胞肺癌亚种群如何通过转化增长因子β1 (TGF-β1) 信号来合作,影响入侵和转移.
科学领域:
- 在瘤学瘤学.
- 细胞生物学 细胞生物学
- 癌症研究 癌症研究
背景情况:
- 内异质性是癌症进展和治疗耐药性的关键驱动因素.
- 癌症中细胞亚群通信的机制仍然不太清楚.
研究的目的:
- 在集体入侵期间,解构非小细胞肺癌 (NSCLC) 亚种群的合作机制.
- 阐明细胞间通信在维持瘤异质性和促进进展中的作用.
主要方法:
- 利用集体入侵作为NSCLC的一个模型系统.
- 在入侵群中分析了异质的循环和非循环亚群.
- 研究了转化生长因子β1 (TGF-β1) 和JAG1信号的作用.
主要成果:
- 集体入侵的NSCLC群包括不同的循环和非循环亚群.
- 追随者亚群分泌TGF-β1,在领导者亚群中诱导上下文依赖的反应.
- TGF-β1在孤立的追随者中促进繁殖,但在孤立的领导者中促进静止;然而,异质群体中的领导者繁殖以保持比例.
- 由TGF-β1.1.刺激的JAG1依赖的入侵.
- 领导者和追随者分群都对体内转移性进展至关重要.
结论:
- 细胞间通信,特别是TGF-β1信号传递,对于保持瘤细胞异质性至关重要.
- 这种沟通促进了NSCLC的集体行为,如入侵和进展.
- 针对这些通讯途径可能为治疗转移性癌症提供治疗策略.
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