Endogenous control mechanisms of FAK and PYK2 and their relevance to cancer development

Rayan Naser, Abdullah Aldehaiman, Escarlet Díaz-Galicia, Stefan T. Arold*

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

46 Scopus citations


Focal adhesion kinase (FAK) and its close paralogue, proline-rich tyrosine kinase 2 (PYK2), are key regulators of aggressive spreading and metastasis of cancer cells. While targeted small-molecule inhibitors of FAK and PYK2 have been found to have promising antitumor activity, their clinical long-term efficacy may be undermined by the strong capacity of cancer cells to evade anti-kinase drugs. In healthy cells, the expression and/or function of FAK and PYK2 is tightly controlled via modulation of gene expression, competing alternatively spliced forms, non-coding RNAs, and proteins that directly or indirectly affect kinase activation or protein stability. The molecular factors involved in this control are frequently deregulated in cancer cells. Here, we review the endogenous mechanisms controlling FAK and PYK2, and with particular focus on how these mechanisms could inspire or improve anticancer therapies.

Original languageEnglish (US)
Article number196
Issue number6
StatePublished - Jun 11 2018


  • Anoikis
  • Chaperon
  • Dimerization
  • FIP200
  • LKB1
  • MiRNA
  • Motility
  • PI3K
  • PTEN
  • Regulation

ASJC Scopus subject areas

  • Oncology
  • Cancer Research


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