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Targeting Splicing in Prostate Cancer
Over 95% of human genes are alternatively spliced, expressing splice isoforms that often exhibit antagonistic functions. We describe genes whose alternative splicing has been linked to prostate cancer; namely VEGFA, KLF6, BCL2L2, ERG, and AR. We discuss opportunities to develop novel therapies that...
Autores principales: | , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5983716/ https://www.ncbi.nlm.nih.gov/pubmed/29693622 http://dx.doi.org/10.3390/ijms19051287 |
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author | Antonopoulou, Effrosyni Ladomery, Michael |
author_facet | Antonopoulou, Effrosyni Ladomery, Michael |
author_sort | Antonopoulou, Effrosyni |
collection | PubMed |
description | Over 95% of human genes are alternatively spliced, expressing splice isoforms that often exhibit antagonistic functions. We describe genes whose alternative splicing has been linked to prostate cancer; namely VEGFA, KLF6, BCL2L2, ERG, and AR. We discuss opportunities to develop novel therapies that target specific splice isoforms, or that target the machinery of splicing. Therapeutic approaches include the development of small molecule inhibitors of splice factor kinases, splice isoform specific siRNAs, and splice switching oligonucleotides. |
format | Online Article Text |
id | pubmed-5983716 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-59837162018-06-05 Targeting Splicing in Prostate Cancer Antonopoulou, Effrosyni Ladomery, Michael Int J Mol Sci Review Over 95% of human genes are alternatively spliced, expressing splice isoforms that often exhibit antagonistic functions. We describe genes whose alternative splicing has been linked to prostate cancer; namely VEGFA, KLF6, BCL2L2, ERG, and AR. We discuss opportunities to develop novel therapies that target specific splice isoforms, or that target the machinery of splicing. Therapeutic approaches include the development of small molecule inhibitors of splice factor kinases, splice isoform specific siRNAs, and splice switching oligonucleotides. MDPI 2018-04-25 /pmc/articles/PMC5983716/ /pubmed/29693622 http://dx.doi.org/10.3390/ijms19051287 Text en © 2018 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Review Antonopoulou, Effrosyni Ladomery, Michael Targeting Splicing in Prostate Cancer |
title | Targeting Splicing in Prostate Cancer |
title_full | Targeting Splicing in Prostate Cancer |
title_fullStr | Targeting Splicing in Prostate Cancer |
title_full_unstemmed | Targeting Splicing in Prostate Cancer |
title_short | Targeting Splicing in Prostate Cancer |
title_sort | targeting splicing in prostate cancer |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5983716/ https://www.ncbi.nlm.nih.gov/pubmed/29693622 http://dx.doi.org/10.3390/ijms19051287 |
work_keys_str_mv | AT antonopouloueffrosyni targetingsplicinginprostatecancer AT ladomerymichael targetingsplicinginprostatecancer |