焦点粘着
血管生成
周细胞
PTK2
癌症研究
受体酪氨酸激酶
酪氨酸激酶
细胞生物学
信号转导
癌变
生物
癌症
蛋白激酶C
内皮干细胞
生物化学
丝裂原活化蛋白激酶激酶
体外
遗传学
作者
Jingyu Zhang,Wěi Li,Wenxin Wang,Qingqing Chen,Zishan Xu,Meijing Deng,Lin Zhou,Guoyang He
标识
DOI:10.1016/j.ejphar.2023.175694
摘要
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.
科研通智能强力驱动
Strongly Powered by AbleSci AI