Endocrine Abstracts (2016) 42 P31 | DOI: 10.1530/endoabs.42.P31

Mediators of stress resistance in prostate cancer cells

Adam Pickard1, Francesca Amoroso1, Lorna May-Stewart1, Jonathan McComb1 & Ian G. Mills1,2,3


1Prostate Cancer UK/Movember Centre of Excellence, Centre for Cancer Research and Cell Biology, Queen’s University Belfast, Belfast, UK; 2Prostate Cancer Research Group, Centre for Molecular Medicine (Norway), University of Oslo and Oslo University Hospitals, Oslo, Norway; 3Department of Molecular Oncology, Institute for Cancer Research, Oslo University Hospitals-Radium Hospital, Montebello, Oslo, Norway


The emergence of prostate cancer and the progression of the disease are significantly driven by the androgen receptor (AR) in combination with other transcription factors. The evolution of aggressive disease requires tumours to become resistant to metabolic stress and subsequently therapeutic stress. Given the role of the prostate gland has a secretory organ characterised by high rates of protein synthesis particularly in AR-positive luminal epithelial cells there are inherent biologies that contribute to stress resistance, notably protein folding. This presentation will outline some example of the AR-dependent pathways which contribute to stress resistance and how these evolve as metastatic disease emerges culminating in pro-inflammatory signalling and immune evasion. At each stage in this process there are opportunities to repurpose therapeutics which may restrict disease progression.

Presenting Author: Ian Mills, Centre for Cancer Research and Cell Biology (CCRCB), Queen’s University of Belfast, BT9 7AE, Belfast, UK. Email: I.Mills@qub.ac.uk

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