Endogenous Control Mechanisms of FAK and PYK2 and Their Relevance to Cancer Development and Therapy
AuthorsNaser, Rayan Mohammad Mahmoud
Diaz Galicia, Miriam Escarlet
Arold, Stefan T.
KAUST DepartmentBiological and Environmental Sciences and Engineering (BESE) Division
Computational Bioscience Research Center (CBRC)
Computer, Electrical and Mathematical Sciences and Engineering (CEMSE) Division
KAUST Grant NumberURF/1/2602-01-01
MetadataShow full item record
AbstractFocal 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 are showing 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 through 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 are frequently deregulated in cancer cells. Here, we review the endogenous mechanisms controlling FAK and PYK2, and discuss how these mechanisms could inspire or improve anticancer therapies.
CitationNaser R, Aldehaiman A, Diaz Galicia ME, Arold ST (2018) Endogenous Control Mechanisms of FAK and PYK2 and Their Relevance to Cancer Development and Therapy. Available: http://dx.doi.org/10.20944/preprints201805.0125.v1.
SponsorsWe thank V. Unkefer for editorial proof reading, and J-A. Girault, S. Hong, B.W.Quereshi and A.A. Momin for suggestions and discussions. This publication was supported by King Abdullah University of Science and Technology (KAUST) through the baseline funds and Award No URF/1/2602-01-01 from the Office of Sponsored Research (OSR).