Phenotypic plasticity in prostate cancer: role of intrinsically disordered proteins

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dc.citation.firstpage704en_US
dc.citation.journalTitleAsian Journal of Andrologyen_US
dc.citation.lastpage710en_US
dc.citation.volumeNumber18en_US
dc.contributor.authorMooney, Steven M.en_US
dc.contributor.authorJolly, Mohit Kumaren_US
dc.contributor.authorLevine, Herberten_US
dc.contributor.authorKulkarni, Prakashen_US
dc.contributor.orgBioengineeringen_US
dc.contributor.orgPhysics and Astronomyen_US
dc.contributor.orgCenter for Theoretical Biological Physicsen_US
dc.date.accessioned2016-09-30T20:52:22Zen_US
dc.date.available2016-09-30T20:52:22Zen_US
dc.date.issued2016en_US
dc.description.abstractA striking characteristic of cancer cells is their remarkable phenotypic plasticity, which is the ability to switch states or phenotypes in response to environmental fluctuations. Phenotypic changes such as a partial or complete epithelial to mesenchymal transition (EMT) that play important roles in their survival and proliferation, and development of resistance to therapeutic treatments, are widely believed to arise due to somatic mutations in the genome. However, there is a growing concern that such a deterministic view is not entirely consistent with multiple lines of evidence, which indicate that stochasticity may also play an important role in driving phenotypic plasticity. Here, we discuss how stochasticity in protein interaction networks (PINs) may play a key role in determining phenotypic plasticity in prostate cancer (PCa). Specifically, we point out that the key players driving transitions among different phenotypes (epithelial, mesenchymal, and hybrid epithelial/mesenchymal), including ZEB1, SNAI1, OVOL1, and OVOL2, are intrinsically disordered proteins (IDPs) and discuss how plasticity at the molecular level may contribute to stochasticity in phenotypic switching by rewiring PINs. We conclude by suggesting that targeting IDPs implicated in EMT in PCa may be a new strategy to gain additional insights and develop novel treatments for this disease, which is the most common form of cancer in adult men.en_US
dc.identifier.citationMooney, Steven M., Jolly, Mohit Kumar, Levine, Herbert, et al.. "Phenotypic plasticity in prostate cancer: role of intrinsically disordered proteins." <i>Asian Journal of Andrology,</i> 18, (2016) Wolters Kluwer: 704-710. http://dx.doi.org/10.4103/1008-682X.183570.en_US
dc.identifier.doihttp://dx.doi.org/10.4103/1008-682X.183570en_US
dc.identifier.urihttps://hdl.handle.net/1911/91627en_US
dc.language.isoengen_US
dc.publisherWolters Kluweren_US
dc.rightsArticle is made available in accordance with the publisher's policy and may be subject to US copyright law. Please refer to the publisher's site for terms of use.en_US
dc.subject.keywordepithelial to mesenchymal transitionen_US
dc.subject.keywordintrinsically disordered proteinsen_US
dc.subject.keywordprostate canceren_US
dc.subject.keywordstate-switchingen_US
dc.titlePhenotypic plasticity in prostate cancer: role of intrinsically disordered proteinsen_US
dc.typeJournal articleen_US
dc.type.dcmiTexten_US
dc.type.publicationpublisher versionen_US
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