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Cancer cell polarization and immune evasion in the niche; co-regulation by the multitasking Focal Adhesion Kinase

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Dates:23 February 2016
Times:13:00 - 14:00
What is it:Seminar
Organiser:Faculty of Life Sciences
Who is it for:University staff, Current University students
Speaker:Professor Margaret Frame
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  • In category "Seminar"
  • In group "(FLS) Tissue Systems Seminar Series"
  • By Faculty of Life Sciences

Part of the Faculty of Life Sciences' Tissue Systems Seminar Series

Margaret C Frame 1, Tom Lund 1*, Bryan Serrels 1, Adam Byron 1, Valerie G Brunton 1, Robert J.B. Nibbs 2, Alan Serrels 1

1 Edinburgh Cancer Research UK Centre, Crewe Road South, University of Edinburgh UK 2 Institute of Infection, Immunity, and Inflammation, University of Glasgow, UK

The behavior of tumors can be ascribed to both cell-autonomous and non cell-autonomous traits. The integrin effector protein Focal Adhesion Kinase (FAK), which is mis-regulated in cancer, is a self-regulating scaffold/ kinase that controls molecular protein complex assembly at adhesion sites and at other sub-cellular locale. Adhesion-linked complexes ‘built’ by FAK typically regulate processes associated with adhesion and actin dynamics, and consequently cancer cell polarization and invasion. However, the tumor niche is composed of multiple cell types – a mini tissue - only a proportion of which are cancer cells. It is in this context that we have now also discovered a completely new function of FAK in driving anti-tumor immune evasion. Specifically, the activity of nuclear-targeted FAK in cancer cells drives recruitment and retention of intra-tumoral regulatory T-cells (Tregs) by transcriptionally regulating chemokine and cytokine ligand-receptor networks, crucially including transcription of Ccl5 and TGFb2. In turn, these changes inhibit antigen-primed cytotoxic CD8+ T-cell activity in the tumor microenvironment, permitting survival and growth of FAK-expressing tumors. We show that immune evasion requires nuclear FAK’s catalytic activity and and small molecule FAK kinase inhibitors drive depletion of Tregs and permit CD8+ T-cell-mediated tumor clearance. It is therefore likely that FAK inhibitors may trigger both inhibition of polarization and invasion, and promote immune-mediated negative pressure on tumours, potentially providing previously unrecognized therapeutic benefits.

Speaker

Professor Margaret Frame

Organisation: Edinburgh Cancer Research Centre

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charlotte.houghton@manchester.ac.uk

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