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Volume 16, Issue 4 (July 2014) 16, 515–521; 10.4103/1008-682X.127825

The role of mRNA splicing in prostate cancer

Anna V Lapuk1, Stanislav V Volik1, Yuzhuo Wang2, Colin C Collins3

1 Vancouver Prostate Centre, University of British Columbia,
2 Vancouver Prostate Centre, University of British Columbia; Department of Experimental Therapeutics, BC Cancer Agency, Vancouver, BC, Canada,
3 Vancouver Prostate Centre; Department of Urologic Sciences, University of British Columbia,

Correspondence: Dr. AV Lapuk (alapuk@prostatecentre.com)

Received: 07 January 2014; Accepted: 12 February 2014


Alternative splicing (AS) is a crucial step in gene expression. It is subject to intricate regulation, and its deregulation in cancer can lead to a wide array of neoplastic phenotypes. A large body of evidence implicates splice isoforms in most if not all hallmarks of cancer, including growth, apoptosis, invasion and metastasis, angiogenesis, and metabolism. AS has important clinical implications since it can be manipulated therapeutically to treat cancer and represents a mechanism of resistance to therapy. In prostate cancer (PCa) AS also plays a prominent role and this review will summarize the current knowledge of alternatively spliced genes with important functional consequences. We will highlight accumulating evidence on AS of the components of the two critical pathways in PCa: androgen receptor (AR) and phosphoinositide 3-kinase (PI3K). These observations together with data on dysregulation of splice factors in PCa suggest that AR and PI3K pathways may be interconnected with previously unappreciated splicing regulatory networks. In addition, we will discuss several lines of evidence implicating splicing regulation in the development of the castration resistance.

Keywords: alternative splicing; prostate cancer; androgen receptor; PI3K pathway; CRPC; neuroendocrine transdifferentiation; REST repressor complex

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