Department of Cancer Genetics, Roswell Park Cancer Institute, Elm and Carlton Streets, Buffalo, NY 14263, USA.
Anticancer Agents Med Chem. 2011 Sep;11(7):607-16. doi: 10.2174/187152011796817646.
Focal adhesion kinase (FAK) is a non-receptor tyrosine kinase which mediates integrin signaling from the sites of connection to the extracellular membrane known as focal adhesions. FAK mediates essential cellular processes including growth, proliferation, adhesion, migration, and survival through its functions as a molecular scaffold and as a kinase. FAK is frequently overexpressed and overactive in prostate cancer, which represents the second leading cause of cancer deaths in American men. Through the activation of major oncogenic pathways, FAK promotes the growth, survival, migration, metastasis, and androgen-independence of prostate tumors in vitro and in vivo. A full examination of FAK kinase function has never been completed despite many studies suggesting its importance and the development of kinase-specific therapeutic inhibitors. An expanded understanding of FAK kinase function is required to understand the role of FAK in prostate cancer progression, thereby aiding future development of novel inhibitory drugs and screening procedures.
黏着斑激酶（FAK）是一种非受体酪氨酸激酶，它介导整合素信号从细胞外膜的连接点传递到称为黏着斑的位置。FAK 通过作为分子支架和激酶的功能，介导包括生长、增殖、黏附、迁移和存活在内的基本细胞过程。FAK 在前列腺癌中经常过度表达和过度活跃，这是美国男性癌症死亡的第二大主要原因。通过激活主要致癌途径，FAK 促进前列腺肿瘤在体外和体内的生长、存活、迁移、转移和雄激素独立性。尽管许多研究表明其重要性和激酶特异性治疗抑制剂的发展，但尚未完成对 FAK 激酶功能的全面检查。需要更深入地了解 FAK 激酶的功能，以了解 FAK 在前列腺癌进展中的作用，从而有助于未来开发新型抑制药物和筛选程序。
