2017 Participants
Kathryn Patterson
The androgen receptor (AR) stimulates PCa cell growth when activated by the binding of the hormone testosterone.
Current therapies avoid AR activation by preventing testosterone binding to the AR. This slows the growth of the PCa tumour. Unfortunately, the AR often develops resistance to such therapies. Changes in the AR structure as a result of gene mutation allow the AR to become activated in the absence of testosterone resulting in tumour growth that cannot be controlled through current therapies.
In addition to testosterone, studies suggest that an alternative cellular component- novel kinase IKBKE- may also play a role in AR regulation. This project aimed to understand the effect of IKBKE inhibition and siRNA knock-down on PCa cell growth to determine if IKBKE has the potential to be a therapeutic target in PCa treatment.
Funding source: Wellcome Trust