| Literature DB >> 19787209 |
Huifang Hao1, Yoshio Naomoto, Xiaohong Bao, Nobuyuki Watanabe, Kazufumi Sakurama, Kazuhiro Noma, Takayuki Motoki, Yasuko Tomono, Takuya Fukazawa, Yasuhiro Shirakawa, Tomoki Yamatsuji, Junji Matsuoka, Z G Wang, Munenori Takaoka.
Abstract
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.Entities:
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Year: 2009 PMID: 19787209 DOI: 10.3892/or_00000524
Source DB: PubMed Journal: Oncol Rep ISSN: 1021-335X Impact factor: 3.906