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微环境使乳腺瘤ECs通过微RNA-200-b-3p调节和细胞外矩阵重塑来实现脱差

Kinga Wilkus-Adamczyk^1,2, Klaudia Brodaczewska¹, Aleksandra Majewska^1,2

¹Laboratory of Molecular Oncology and Innovative Therapies, Military Institute of Medicine- National Research Institute, Warsaw, Poland.

Frontiers in cell and developmental biology

|June 1, 2023

概括

瘤微环境缺氧会改变内皮细胞 (EC) 迁移和基因表达,促进癌症中的内皮细胞转移到介质细胞 (EndMT). 瘤ECs中的MiR-200b-3p上调驱动EndMT并沉默血管生成因子.

科学领域:

在瘤学瘤学.
细胞生物学细胞生物学
分子生物学分子生物学

背景情况:

缺氧是瘤微环境的关键因素,影响癌症进展和血管生成.
内皮细胞 (ECs) 是瘤内病理血管生成的关键参与者.
与健康的EC相比,来自瘤的EC表现出不同的反应,特别是在内皮转移到介质酶转移 (EndMT) 期间.

研究的目的:

研究瘤微环境对ECs全球基因表达模式的影响.
在EndMT期间,比较瘤衍生EC与健康EC的不同反应.
阐明miR-200b-3p在EndMT中的调节作用及其对癌症EC行为的影响.

主要方法:

使用了从健康乳腺组织 (HBH.MEC) 和乳腺癌 (HBCa.MEC) 中获得的不朽化EC线.
在正常氧和缺氧 (48h) 条件下进行实验,以评估EC迁移 (伤口愈合试验).
进行了全球基因表达分析 (NGS) 和miRNA分析,通过qPCR和miR-200b-3p模仿实验验证实结果.

主要成果:

缺氧不同影响了EC迁移;健康的EC减缓了,而瘤EC由于EndMT而保持了迁移.
在癌症EC中,NGS揭示了改变的细胞外矩阵 (ECM) 组织,具有验证的放松调节基因,包括SPP1,ITGB6,COL4A4等.
确定了miR-200b-3p在瘤EC中显著上调,这表明它在调节EndMT和静止血管性因素方面的作用.

结论:

病理性ECs与正常ECs表现出明显的表型和功能差异,影响瘤微环境相互作用.
基因表达特征证实EndMT在瘤衍生的EC中,导致增强的迁移性质.
miR-200b-3p通过向血管生长因子及其受体,在病理性EC中调节EndMT方面发挥着至关重要的作用.

关键词:

ECM-受体相互作用 (细胞外矩阵-受体相互作用)乳腺癌乳腺癌乳腺癌脑内皮细胞 (ECs) 是一种内皮细胞.从内皮转移到介质细胞转变 (EndMT)异质性的异质性在 miR-200b-3p 中使用.

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