Targeting FAK in anticancer combination therapies.
Targeting FAK in anticancer combination therapies.
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DOI：
10.1038/s41568-021-00340-6
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发表时间：
2021-05
期刊：
影响因子：
--
通讯作者：
Frame MC
中科院分区：
文献类型：
--
作者：
Dawson JC;Serrels A;Stupack DG;Schlaepfer DD;Frame MC
局灶黏附激酶（Focal adhesion kinase， FAK）是一种非受体酪氨酸激酶，也是一种主要调节黏附信号和细胞迁移的衔接蛋白，但FAK也可以促进细胞在应激反应中的存活。FAK通过其激酶和支架功能介导多种癌细胞功能。它通常在癌症中过度表达，被认为是一种高价值的药物治疗靶点，目前有多种FAK激酶抑制剂正在开发中。大量证据表明，作为临床联合策略，FAK靶向治疗将是最有效的，从而逆转化疗或靶向治疗的失败，提高实体瘤免疫治疗的疗效。在这里，我们讨论了最近的临床前证据，这些证据表明FAK与抗癌治疗耐药有关，从而得出FAK激酶抑制剂将在分层情况下作为联合治疗具有最大效用的观点。
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 impacts on a diverse range of cancer cell functions mediated by both its kinase and scaffolding functions. It is commonly overexpressed in cancer and has been considered a high value druggable target for therapy, with multiple FAK kinase inhibitors currently in development. Substantial evidence has emerged implying that it is as clinical combination strategies that FAK targeting will be most effective, 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 pre-clinical evidence that implicates FAK in anti-cancer therapeutic resistance, leading to the view that FAK kinase inhibitors will have their greatest utility as combination therapies in stratified contexts.
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DOI：
10.4049/jimmunol.1301587
发表时间：
2013-12-15
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
--
作者：
Chapman NM;Connolly SF;Reinl EL;Houtman JC
通讯作者：
Houtman JC
影响因子：
7.7
作者：
Canel, Marta;Taggart, David;Serrels, Alan
通讯作者：
Serrels, Alan
影响因子：
16
作者：
Courtney AH;Amacher JF;Kadlecek TA;Mollenauer MN;Au-Yeung BB;Kuriyan J;Weiss A
通讯作者：
Weiss A
影响因子：
11.4
作者：
Acebron, Ivan;Righetto, Ricardo D.;Lietha, Daniel
通讯作者：
Lietha, Daniel
影响因子：
7.7
作者：
Diaz Osterman, Carlos J.;Ozmadenci, Duygu;Schlaepfer, David D.
通讯作者：
Schlaepfer, David D.