Focal Adhesion Kinase Controls Prostate Cancer Progression Via Intrinsic Kinase and Scaffolding Functions
Focal Adhesion Kinase Controls Prostate Cancer Progression Via Intrinsic Kinase and Scaffolding Functions
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DOI：
10.2174/187152011796817646
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发表时间：
2011-09-01
影响因子：
2.8
通讯作者：
Gelman, Irwin H.
中科院分区：
文献类型：
--
作者：
Figel, Sheila;Gelman, Irwin H.
粘着斑激酶(FAK)是一种非受体酪氨酸激酶，它介导从连接部位到细胞外膜的整合素信号，称为粘着斑。FAK通过其作为分子支架和作为一种激酶的功能，调节包括生长、增殖、黏附、迁移和生存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，前列腺癌是美国男性癌症死亡的第二大原因。通过激活主要的致癌途径，FAK在体内外促进前列腺癌的生长、存活、迁移、转移和雄激素非依赖性。尽管有许多研究表明了FAK的重要性和开发专门的治疗抑制剂，但对FAK激酶功能的全面检查一直没有完成。为了了解FAK在前列腺癌进展中的作用，需要对FAK的功能有更深入的了解，从而有助于未来开发新的抑制药物和筛选程序。
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.