FAK regulates biological processes important for the pathogenesis of cancer

被引：318

作者：

Gabarra-Niecko, V

Schaller, MD ^{[1
]}

Dunty, JM

机构：

[1] Univ N Carolina, Dept Cell & Dev Biol, Chapel Hill, NC 27599 USA

[2] Univ N Carolina, Lineberger Comprehens Canc Ctr, Chapel Hill, NC 27599 USA

[3] Univ N Carolina, Comprehens Ctr Inflammatory Disorders, Chapel Hill, NC 27599 USA

[4] Univ N Carolina, Ctr Thrombosis & Hemostasis, Chapel Hill, NC 27599 USA

来源：

CANCER AND METASTASIS REVIEWS | 2003年 / 22卷 / 04期

关键词：

focal adhesion kinase; signaling; cancer;

D O I：

10.1023/A:1023725029589

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Since its initial discovery as a substrate and binding partner for the Src oncogene, a role for the focal adhesion kinase (FAK) in cancer has been speculated. In this review the clinical evidence correlating FAK overexpression with cancer and the experimental evidence demonstrating that FAK can control some phenotypes associated with cancer will be discussed. In addition, the emerging theme of interactions between the FAK and growth factor signaling pathways will be described. The evidence presented in this review provides a compelling case for a role for FAK in the pathology of human cancer.

引用

页码：359 / 374

页数：16

共 110 条

[1] Focal adhesion kinase activated by β4 integrin ligation to mCLCA1 mediates early metastatic growth [J].