Translational interrogations of prostate cancer
Prostate cancer (PrCa) is a leading cause of cancer related male mortality in the United Kingdom with over 10,000 deaths each year.
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Funding sourceUniversity of Surrey
The growth and progression of PrCa is regulated by androgens, which manifest their action by activating the androgen receptor (AR), a ligand activated transcription factor that in turn regulates the growth of PrCa. Since AR signaling is upregulated in PrCa, it is an attractive drug target in the treatment of the advanced PrCa. Hence, widely used androgen deprivation therapy (ADT) is the mainstay treatment for PrCa, which is achieved by the use of anti-androgenic drugs such as Bicalutamide and Enzalutamide. ADT is initially effective but relapse is common leading to castration resistant prostate cancer (CRPC) for which there are no curative treatments. The key question is why does ADT fail and how can we develop more effective anti-androgens to target the AR? In collaboration with the Department of Chemistry University of Cambridge and Nuffield Department of Surgical Sciences, University of Oxford, this project will discover novel anti-androgens to develop curative treatment for CRPC. The findings of this study will pave the way to effectively treat CRPC in order to alleviate the disease burden.
(1) Kinase joins the chaperone club: Androgen-regulated kinome reveals choline kinase alpha as a potential drug target in prostate cancer. Asim M, Massie CE, Neal DE. Mol Cell Oncol. 2016 Feb 24;3(3).
(2) Choline Kinase Alpha as an Androgen Receptor Chaperone and Prostate Cancer Therapeutic Target. Asim M, Massie CE, (………) Neal DE. J Natl Cancer Inst. 2015 Dec 11;108(5).
(3) Ligand-dependent corepressor acts as a novel androgen receptor corepressor, inhibits prostate cancer growth, and is functionally inactivated by the Src protein kinase. Asim M, (….) Baniahmad A. J Biol Chem. 2011 Oct 28;286(43):37108-17.
(4) Src kinase potentiates androgen receptor transactivation function and invasion of androgen-independent prostate cancer C4-2 cells. Asim M, Siddiqui IA, Hafeez BB, Baniahmad A, Mukhtar H. Oncogene. 2008 Jun 5;27(25):3596-604.
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