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Blood vessel formation starts early during embryonic development, around day 7. In the extraembryonic yolk sac, mesodermal precursor cells called hemangioblast proliferate and differentiate into angioblast. Angioblasts express vascular endothelial growth factor receptor 2 or VEGFR2, which binds VEGF-A, a proangiogenic factor, guiding blood vessel formation. VEGF signaling promotes angioblasts to form a blood island in the developing embryo. Angioblasts further differentiate, giving rise to...
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    转录因子HOXD13通过增强血管形成和抑制抗瘤T细胞来促进黑色素瘤的生长. 抑制它的点,VEGF和腺受体,在模型中逆转了这种效应.

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    科学领域:

    • 分子生物学分子生物学
    • 癌症研究 癌症研究
    • 免疫学 免疫学 免疫学

    背景情况:

    • 紫外线辐射诱导的DNA突变驱动黑色素瘤的启动和新抗原的形成,触发抗瘤免疫力.
    • 黑色素瘤细胞通过调节表观遗传学和瘤微环境相互作用,包括血管生成来逃避免疫检测.
    • 瘤增强血液流动,同时防止免疫细胞透,这是一个复杂的过程,涉及免疫逃避策略.

    研究的目的:

    • 研究转录因子 (TFs) 在黑色素瘤发育和免疫逃避中的作用.
    • 在黑色素瘤中识别与血管生成和免疫细胞排除相关的特定TFs.
    • 阐明HOXD13影响瘤生长,血管生成和免疫抑制的分子机制.

    主要方法:

    • 在早期黑色素瘤,纳维和其他癌症中对TF表达的比较分析.
    • 转录学,3D染色体分析,以及体内黑色素瘤模型.
    • 评估HOXD13对血管生成,T细胞透和基因调节的影响.

    主要成果:

    • 在黑色素瘤中,HOXD13的上调驱动着类似于黑色素细胞的程序,与血管生成的增加和抑制的T细胞透有关.
    • 通过编排3D染色质接触,HOXD13激活VEGFA,SEMA3A和CD73,促进瘤生长.
    • 维格法和SEMA3A重塑血管系统;CD73提高腺,一个血管扩张和免疫抑制剂.

    结论:

    • 在黑色素瘤中,HOXD13建立了一个双重的亲血管和免疫抑制轴 (HOXD13-CD73/VEGF).
    • 在体内,HOXD13诱导的瘤生长被VEGFR和腺素受体 (AdR) 的联合抑制逆转.
    • 确定潜在受益于联合AdR和VEGFR抑制剂治疗的患者子组.