Nuclear FAK and Runx1 cooperate to regulate IGFBP3, cell cycle progression and tumor growth

Research output: Contribution to journalArticlepeer-review

Abstract

Nuclear focal adhesion kinase (FAK) is a potentially important regulator of gene
expression in cancer, impacting both cellular function and the composition of the surrounding tumor microenvironment. Here we report in a murine model of skin squamous cell carcinoma (SCC) that nuclear FAK regulates Runx1-dependent transcription of insulin-like growth factor binding protein 3 (IGFBP3), and that this regulates SCC cell cycle progression and tumor growth in vivo. Furthermore, we identified a novel molecular complex between FAK and Runx1 in the nucleus of SCC cells and showed that FAK interacted with a number of Runx1 regulatory proteins, including Sin3a and other epigenetic modifiers known to alter Runx1 transcriptional function through post-translational modification. These findings provide important new insights into the role of FAK as a scaffolding protein in molecular complexes that regulate gene transcription.
Original languageEnglish
Pages (from-to)5301-5312
JournalCancer Research
Volume77
Issue number19
Early online date14 Aug 2017
DOIs
Publication statusPublished - 1 Oct 2017

Fingerprint Dive into the research topics of 'Nuclear FAK and Runx1 cooperate to regulate IGFBP3, cell cycle progression and tumor growth'. Together they form a unique fingerprint.

Cite this