Focal adhesion kinase as potential target for cancer therapy

Huifang Hao, 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

Research output: Contribution to journalReview articlepeer-review

55 Citations (Scopus)


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.

Original languageEnglish
Pages (from-to)973-979
Number of pages7
JournalOncology reports
Issue number5
Publication statusPublished - 2009


  • FAK inhibitor
  • FAK-related non-kinase
  • FERM
  • Focal adhesion kinase

ASJC Scopus subject areas

  • Oncology
  • Cancer Research


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