Phenotypic plasticity in prostate cancer: role of intrinsically disordered proteins

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dc.citation.firstpage704
dc.citation.journalTitleAsian Journal of Andrology
dc.citation.lastpage710
dc.citation.volumeNumber18
dc.contributor.authorMooney, Steven M.
dc.contributor.authorJolly, Mohit Kumar
dc.contributor.authorLevine, Herbert
dc.contributor.authorKulkarni, Prakash
dc.contributor.orgCenter for Theoretical Biological Physics
dc.date.accessioned2016-09-30T20:52:22Z
dc.date.available2016-09-30T20:52:22Z
dc.date.issued2016
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.
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.
dc.identifier.doihttp://dx.doi.org/10.4103/1008-682X.183570
dc.identifier.urihttps://hdl.handle.net/1911/91627
dc.language.isoeng
dc.publisherWolters Kluwer
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.
dc.subject.keywordepithelial to mesenchymal transition
dc.subject.keywordintrinsically disordered proteins
dc.subject.keywordprostate cancer
dc.subject.keywordstate-switching
dc.titlePhenotypic plasticity in prostate cancer: role of intrinsically disordered proteins
dc.typeJournal article
dc.type.dcmiText
dc.type.publicationpublisher version
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