Abstract：
Focal adhesion kinase (FAK), also known as protein tyrosine kinase 2 (PTK2), is a ubiquitously expressed non-receptor tyrosine kinase, that plays a pivotal role in integrin-mediated signal transduction. Endothelial FAK is upregulated in many types of cancer and promotes tumorigenesis and tumor progression. However, recent studies have shown that pericyte FAK has the opposite effect. This review article dissects the mechanisms, by which endothelial cells (ECs) and pericyte FAK regulate angiogenesis, with an emphasis on the Gas6/Axl pathway. In particular, this article discusses the role of pericyte FAK loss on angiogenesis during tumorigenesis and metastasis. In addition, the existing challenges and future application of drug-based anti-FAK targeted therapies will be discussed to provide a theoretical basis for further development and use of FAK inhibitors.
摘要：
粘着斑激酶(FAK),也称为蛋白酪氨酸激酶2（PTK2），是一种广泛表达的非受体酪氨酸激酶，在整合素介导的信号转导中起着关键作用。内皮FAK在许多类型的癌症中上调并促进肿瘤发生和肿瘤进展。然而,最近的研究表明，周细胞FAK具有相反的效果。这篇综述文章剖析了机制，内皮细胞（ECs）和周细胞FAK调节血管生成，重点是Gas6/Axl途径。特别是,本文讨论了周细胞FAK丢失在肿瘤发生和转移过程中对血管生成的作用。此外,将讨论基于药物的抗FAK靶向治疗的现有挑战和未来应用，为FAK抑制剂的进一步开发和使用提供理论依据。
