Hao Huifang, Naomoto Yoshio, Bao Xiaohong, Watanabe Nobuyuki, Sakurama Kazufumi, Noma Kazuhiro, Motoki Takayuki, Tomono Yasuko, Fukazawa Takuya, Shirakawa Yasuhiro, Yamatsuji Tomoki, Matsuoka Junji, Wang Z G, Takaoka Munenori
Department of Gastroenterological Surgery, Transplant and Surgical Oncology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University, Okayama 700-8558, Japan.
Oncol Rep. 2009 Nov;22(5):973-9. doi: 10.3892/or_00000524.
Focal adhesion kinase (FAK) is a 125-kDa non-receptor and non-membrane protein tyrosine. FAK can function with integrins and growth factor receptors to promote cell survival dependent kinase activity and nuclear FAK promotes cell proliferation and survival through FERM (FAK, ezrin, radixin, moesin) domain-enhanced p53 degradation independent kinase activity. Many previous studies have indicated that FAK plays a critical role in the biological processes of normal and cancer cells and FAK has been proposed as a potential target in cancer therapy. Small molecule inhibitors (PF-573,228; PF-562,271 and NVP-226) for use as potential cancer therapies have been developed. However, the detailed mechanism of the role for FAK in tumor cell generation and progression remain unclear, so future work is needed to explore these issues. New inhibitors that can be effectively inhibit the function of FAK still need to be explored due to the low specificity, and resistance.
粘着斑激酶（FAK）是一种125千道尔顿的非受体和非膜蛋白酪氨酸。FAK可与整合素和生长因子受体共同发挥作用，以促进依赖激酶活性的细胞存活，而细胞核中的FAK则通过FERM（FAK、埃兹蛋白、根蛋白、膜突蛋白）结构域增强的p53降解非依赖激酶活性来促进细胞增殖和存活。许多先前的研究表明，FAK在正常细胞和癌细胞的生物学过程中起关键作用，并且FAK已被提议作为癌症治疗的潜在靶点。已经开发出用作潜在癌症治疗药物的小分子抑制剂（PF-573,228、PF-562,271和NVP-226）。然而，FAK在肿瘤细胞产生和进展中作用的详细机制仍不清楚，因此需要未来的工作来探索这些问题。由于特异性低和耐药性，仍需要探索能够有效抑制FAK功能的新型抑制剂。
