Pharmacological perturbation of p68 - an important androgen receptor transcriptional co-regulator in prostate cancer

Prof Craig Robson & Dr Emma Clark, Northern Institute for Cancer Research (NICR), Newcastle University

Approximately 80% of patients who have prostate cancer that is initially treated by removal of the circulating androgen hormone testosterone develop a more aggressive prostate cancer that grows in the absence of androgens. Unfortunately these patients no longer respond to treatment by hormone removal, frequently resulting in death. A current theme of prostate cancer research aims to find effective alternative treatment regimes for these types of prostate cancer.

The normal growth and function of prostate cells is dependant upon the androgenic hormone testosterone which acts upon a factor known as the androgen receptor. Androgens ‘switch on’ the androgen receptor in normal prostate cells, causing these cells to grow and divide. However, in aggressive prostate cancer (which grows in the absence of androgen), androgen receptor function continues to be maintained by other ‘helper’ factors which are able to keep the androgen receptor ‘switched on’ even though androgen is not present.

We have identified one important ‘helper’ factor called the p68 protein which is present at high levels in aggressive prostate cancer. This study aims to understand the functional relationship between p68 and the androgen receptor in the growth of prostate cancer cells, and to test the effectiveness of an established anti-cancer drug called ‘Imatinib’ to inhibit p68 function and to prevent prostate cancer growth. Ultimately, this study will be important in determining the effectiveness of Imatinib as a potential therapy for prostate cancer treatment.

Project commenced
January 2009

Length of project
2 years

Amount Supported
£99,941