Preprint Review Version 1 This version is not peer-reviewed

Endogenous Control Mechanisms of FAK and PYK2 and Their Relevance to Cancer Development and Therapy

Version 1 : Received: 7 May 2018 / Approved: 8 May 2018 / Online: 8 May 2018 (09:07:58 CEST)

A peer-reviewed article of this Preprint also exists.

Naser, R.; Aldehaiman, A.; Díaz-Galicia, E.; Arold, S.T. Endogenous Control Mechanisms of FAK and PYK2 and Their Relevance to Cancer Development. Cancers 2018, 10, 196. Naser, R.; Aldehaiman, A.; Díaz-Galicia, E.; Arold, S.T. Endogenous Control Mechanisms of FAK and PYK2 and Their Relevance to Cancer Development. Cancers 2018, 10, 196.

Journal reference: Cancers 2018, 10, 196
DOI: 10.3390/cancers10060196

Abstract

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 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.

Subject Areas

dimerization; miRNA; motility; anoikis; chaperon; PTEN; FIP200; LKB1; PI3K; regulation

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