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Genes 2017, 8(2), 71; doi:10.3390/genes8020071

Therapeutic Approaches Targeting MYC-Driven Prostate Cancer

1,2
,
3,4,5,6,* , 3,4,5,6,7,8,* and 1,2,4,*
1
Prostate Cancer Translational Research Laboratory, Peter MacCallum Cancer Centre, Melbourne, VIC 3000, Australia
2
Cancer Program, Biomedicine Discovery Institute and Department of Anatomy & Developmental Biology, Monash University, Melbourne, VIC 3800, Australia
3
Oncogenic Signalling and Growth Control Program, Peter MacCallum Cancer Centre, Melbourne, VIC 3000, Australia
4
Sir Peter MacCallum Department of Oncology, University of Melbourne, Parkville, VIC 3010, Australia
5
Department of Biochemistry and Molecular Biology, University of Melbourne, Parkville, VIC 3010, Australia
6
Department of Biochemistry and Molecular Biology, Monash University, Melbourne, VIC 3800, Australia
7
The ACRF Department of Cancer Biology and Therapeutics, The John Curtin School of Medical Research, The Australian National University, Acton, ACT 2601, Australia
8
School of Biomedical Sciences, University of Queensland, Brisbane, QLD 4072, Australia
*
Authors to whom correspondence should be addressed.
Academic Editor: Daitoku Sakamuro
Received: 21 December 2016 / Revised: 6 February 2017 / Accepted: 9 February 2017 / Published: 16 February 2017
(This article belongs to the Special Issue MYC Networks)
View Full-Text   |   Download PDF [703 KB, uploaded 16 February 2017]   |  

Abstract

The transcript encoding the proto-oncogene MYC is commonly overexpressed in prostate cancer (PC). MYC protein abundance is also increased in the majority of cases of advanced and metastatic castrate-resistant PC (mCRPC). Accordingly, the MYC-directed transcriptional program directly contributes to PC by upregulating the expression of a number of pro-tumorigenic factors involved in cell growth and proliferation. A key cellular process downstream of MYC activity is the regulation of ribosome biogenesis which sustains tumor growth. MYC activity also cooperates with the dysregulation of the phosphoinositol-3-kinase (PI3K)/AKT/mTOR pathway to promote PC cell survival. Recent advances in the understanding of these interactions through the use of animal models have provided significant insight into the therapeutic efficacy of targeting MYC activity by interfering with its transcriptional program, and indirectly by targeting downstream cellular events linked to MYC transformation potential. View Full-Text
Keywords: MYC; therapy; prostate cancer; mouse models MYC; therapy; prostate cancer; mouse models
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Rebello, R.J.; Pearson, R.B.; Hannan, R.D.; Furic, L. Therapeutic Approaches Targeting MYC-Driven Prostate Cancer. Genes 2017, 8, 71.

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