<br>FOXC2 促进血管生成拟态和对抗血管生成治疗的抵抗,Cell Reports

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FOXC2 促进血管生成拟态和对抗血管生成治疗的抵抗
Cell Reports ( IF 7.5 ) Pub Date : 2023-07-26 , DOI: 10.1016/j.celrep.2023.112791
Ian G Cannell ₁ , Kirsty Sawicka ₁ , Isabella Pearsall ₁ , Sophia A Wild ₂ , Lauren Deighton ₂ , Sarah M Pearsall ₃ , Giulia Lerda ₂ , Fadwa Joud ₂ , Showkhin Khan ₄ , Alejandra Bruna ₅ , Kathryn L Simpson ₆ , Claire M Mulvey ₂ , Fiona Nugent ₂ , Fatime Qosaj ₂ , Dario Bressan ₂ , ₇ , Caroline Dive ₆ , Carlos Caldas ₈ , Gregory J Hannon ₁

Affiliation

Cancer Research UK Cambridge Institute, University of Cambridge, Li Ka Shing Centre, Robinson Way, Cambridge CB2 0RE, UK; New York Genome Center, 101 Avenue of the Americas, New York, NY 10013, USA.
Cancer Research UK Cambridge Institute, University of Cambridge, Li Ka Shing Centre, Robinson Way, Cambridge CB2 0RE, UK.
Cancer Research UK Cambridge Institute, University of Cambridge, Li Ka Shing Centre, Robinson Way, Cambridge CB2 0RE, UK; Cancer Research UK Cancer Biomarker Centre, Manchester M20 4BX, UK; CRUK Manchester Institute, Manchester M20 4BX, UK.
New York Genome Center, 101 Avenue of the Americas, New York, NY 10013, USA.
Cancer Research UK Cambridge Institute, University of Cambridge, Li Ka Shing Centre, Robinson Way, Cambridge CB2 0RE, UK; Preclinical Modelling of Paediatric Cancer Evolution Team, The Institute of Cancer Research, Cotswold Road, Sutton, Surrey SM2 5N, UK.
Cancer Research UK Cancer Biomarker Centre, Manchester M20 4BX, UK; CRUK Manchester Institute, Manchester M20 4BX, UK.
CRUK IMAXT Grand Challenge Team, Cambridge, UK.
Cancer Research UK Cambridge Institute, University of Cambridge, Li Ka Shing Centre, Robinson Way, Cambridge CB2 0RE, UK; Department of Oncology and Breast Cancer Programme, CRUK Cambridge Centre, Cambridge University Hospitals NHS and University of Cambridge, Cambridge CB2 2QQ, UK.

血管生成拟态（VM）描述了由已获得内皮样特性的肿瘤细胞构建的假血管的形成。 VM通道赋予肿瘤直接连接宿主血管的肿瘤源性血管系统，它们的存在通常与患者预后不良有关。在这里，我们发现转录因子 Foxc2 通过驱动肿瘤细胞内皮基因的异位表达（缺氧刺激的过程）来促进多种实体瘤类型中的 VM。 VM 丰富的肿瘤对抗血管生成治疗有抵抗力，而 Foxc2 的抑制会增强反应。这项工作确立了肿瘤细胞对胚胎内皮转录因子的共同选择作为驱动 VM 倾向的关键机制，并激发了对 VM 抑制药物的研究，这些药物可以构成与抗血管生成药物联合治疗的基础。

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更新日期：2023-07-26

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