Targeting CDK9: a promising therapeutic opportunity in prostate cancer
- Muhammed H Rahaman*,
- Malika Kumarasiri*,
- Laychiluh B Mekonnen,
- Mingfeng Yu,
- Sarah Diab,
- Hugo Albrecht,
- Robert W Milne and
- Shudong Wang⇑
- Centre for Drug Discovery and Development, Sansom Institute for Health Research and School of Pharmacy and Medical Sciences, University of South Australia, Adelaide, South Australia, Australia
- Correspondence should be addressed to S Wang; Email: shudong.wang{at}unisa.edu.au
Abstract
Cyclin-dependent kinase 9 (CDK9) is a key transcriptional regulator and a lucrative target for cancer treatment. Targeting CDK9 can effectively confine the hyperactivity of androgen receptor and the constitutive expression of anti-apoptotic proteins; both being main causes of prostate cancer (PCa) development and progression. In castrate-resistant PCa, traditional therapies that only target androgen receptor (AR) have become obsolete due to reprograming in AR activity to make the cells independent of androgen. CDK9 inhibitors may provide a new and better therapeutic opportunity over traditional treatment options by targeting both androgen receptor activity and anti-apoptotic proteins, improving the chances of positive outcomes, especially in patients with the advanced disease. This review focuses on biological functions of CDK9, its involvement with AR and the potential for therapeutic opportunities in PCa treatment.
- Received 25 August 2016
- Accepted 31 August 2016
- Made available online as an Accepted Preprint 31 August 2016
- © 2016 Society for Endocrinology
