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

Marta Canel, Adam Byron, Andrew H. Sims, Jessy Cartier, Hitesh Patel, Margaret C. Frame, Valerie G. Brunton, Bryan Serrels, Alan Serrels

Research output: Contribution to journalArticlepeer-review

Abstract / Description of output

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
Issue number19
Early online date14 Aug 2017
Publication statusPublished - 1 Oct 2017


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