Journal
CANCERS
Volume 10, Issue 6, Pages -Publisher
MDPI
DOI: 10.3390/cancers10060196
Keywords
dimerization; miRNA; motility; anoikis; chaperon; PTEN; FIP200; LKB1; PI3K; regulation
Categories
Funding
- King Abdullah University of Science and Technology (KAUST)
- Office of Sponsored Research (OSR) [URF/1/2602-01-01]
Ask authors/readers for more resources
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.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available