文章：

靶向FAK的抗癌联合治疗

Targeting FAK in anticancer combination therapies

原文发布日期：2021-03-17

DOI: 10.1038/s41568-021-00340-6

类型: Review Article

开放获取: 否

英文摘要：

Focal adhesion kinase (FAK) is both a non-receptor tyrosine kinase and an adaptor protein that primarily regulates adhesion signalling and cell migration, but FAK can also promote cell survival in response to stress. FAK is commonly overexpressed in cancer and is considered a high-value druggable target, with multiple FAK inhibitors currently in development. Evidence suggests that in the clinical setting, FAK targeting will be most effective in combination with other agents so as to reverse failure of chemotherapies or targeted therapies and enhance efficacy of immune-based treatments of solid tumours. Here, we discuss the recent preclinical evidence that implicates FAK in anticancer therapeutic resistance, leading to the view that FAK inhibitors will have their greatest utility as combination therapies in selected patient populations.

摘要翻译： 

黏着斑激酶（FAK）既是一种非受体酪氨酸激酶，也是一种适配蛋白，主要调控黏附信号传导和细胞迁移，但FAK也能在应激状态下促进细胞存活。FAK在癌症中常过度表达，被视为高价值的药物靶点，目前已有多种FAK抑制剂处于研发阶段。证据表明在临床环境中，FAK靶向治疗与其他药物联用最为有效，可逆转化疗或靶向治疗失败案例，并增强实体瘤免疫治疗的疗效。本文重点讨论了近期关于FAK参与抗癌治疗耐药性的临床前证据，由此认为FAK抑制剂在特定患者群体中作为联合疗法将发挥最大效用。

原文链接：

Targeting FAK in anticancer combination therapies