Focal adhesion kinase as potential target for cancer therapy (Review)

被引：76

作者：

Hao, Huifang ^{[1
]}

Naomoto, Yoshio ^{[1
]}

Bao, Xiaohong ^{[1
]}

Watanabe, Nobuyuki ^{[1
]}

Sakurama, Kazufumi ^{[1
]}

Noma, Kazuhiro ^{[1
]}

Motoki, Takayuki ^{[1
]}

Tomono, Yasuko ^{[2
]}

Fukazawa, Takuya ^{[1
]}

Shirakawa, Yasuhiro ^{[1
]}

Yamatsuji, Tomoki ^{[1
]}

Matsuoka, Junji ^{[1
]}

Wang, Z. G. ^{[3
]}

Takaoka, Munenori ^{[1
]}

机构：

[1] Okayama Univ, Dept Gastroenterol Surg Transplant & Surg Oncol, Grad Sch Med Dent & Pharmaceut Sci, Okayama 7008558, Japan

[2] Shigei Med Res Inst, Okayama, Japan

[3] Inner Mongolia Univ, Coll Life Sci, Key Lab Mammal Reprod Biol & Biotechnol, Minist Educ, Hohhot, Peoples R China

来源：

ONCOLOGY REPORTS | 2009年 / 22卷 / 05期

关键词：

focal adhesion kinase; FAK-related non-kinase; FERM; FAK inhibitor; PROTEIN-TYROSINE KINASE; C-TERMINAL DOMAIN; PROMOTED CELL-MIGRATION; HUMAN TUMOR-CELLS; GROWTH-FACTOR; EXTRACELLULAR-MATRIX; IN-VIVO; SURVIVAL SIGNALS; FAK EXPRESSION; ENDOTHELIAL-CELLS;

D O I：

10.3892/or_00000524

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

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.

引用

页码：973 / 979

页数：7

共 103 条

[1] Matrix survival signaling:: From fibronectin via focal adhesion kinase to c-Jun NH2-terminal kinase [J].