癌症相关的纤维细胞由内皮转化为介质细胞过渡产生的:诱导因子,功能作用和转录基因证据
Junyeol Han1,2, Eung-Gook Kim3, Bo Yeon Kim1,2
1Chemical Biology Research Center, Korea Research Institute of Bioscience and Biotechnology, Cheongju 28116, Republic of Korea.
Biology
|October 29, 2025
概括
内皮转移到介质细胞 (EndMT) 生成与癌症相关的纤维细胞 (CAF),这些纤维细胞驱动瘤生长和治疗耐药性. 本综述详细介绍了EndMT诱导方法及其对瘤微环境 (TME) 的影响.
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:
- 癌症相关纤维细胞 (CAF) 在瘤微环境 (TME) 中至关重要,通过细胞外基质 (ECM) 重塑和细胞因子分泌影响癌症的进展.
- 人们越来越认识到内皮转移到介质酶转移 (EndMT) 是CAFs多样化起源的重要贡献者.
研究的目的:
- 在癌症模型中审查各种诱导EndMT的方法.
- 通过转录和蛋白质组数据总结EndMT细胞类型的证据.
- 讨论癌症诱导EndMT对瘤进展和治疗耐药性的机制和后果.
主要方法:
- 在癌症-小鼠瘤模型中通过条件介质治疗,共同培养,基因扰动,联结体刺激,外体暴露,辐射,病毒感染和3D培养系统诱导EndMT.
- 转录和蛋白质组分析以确定EndMT细胞类型证据.
- 关于EndMT所涉及的报道信号通路和细胞机制的文献综述.
主要成果:
- 标志性EndMT特征包括改变形态,增加运动性,血管新生受损,内皮标记物减少 (CD31,VE-cadherin) 和中细胞标记物增加 (α-SMA,FN1).
- 在EndMT中涉及的关键信号通路包括TGF-β,氧化应激和NOTCH信号.
- 癌症诱导的EndMT促进瘤生长,转移,癌症干细胞的扩张,巨细胞的分化,并与生存率低下和治疗耐药性有关.
结论:
- 终结MT是一个关键的过程,有助于CAF异质性和影响瘤进展.
- 了解EndMT机制和后果对于开发新型癌症疗法至关重要.
- 研究观点在EndMT主要产生CAF还是影响内皮膜屏障功能和转移方面存在差异.
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