dc.contributor.author | Jia, Dongya Jolly, Mohit Kumar Boareto, Marcelo Parsana, Princy Mooney, Steven M. Pienta, Kenneth J. Levine, Herbert Ben-Jacob, Eshel
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dc.date.accessioned |
2016-06-22T16:28:31Z
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dc.date.available |
2016-06-22T16:28:31Z
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dc.date.issued |
2015
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dc.identifier.citation |
Jia, Dongya, Jolly, Mohit Kumar, Boareto, Marcelo, et al.. "OVOL guides the epithelial-hybrid-mesenchymal transition." Oncotarget, 6, no. 17 (2015) Impact Journals, LLC: 15436-15448. http://dx.doi.org/10.18632/oncotarget.3623.
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dc.identifier.uri | https://hdl.handle.net/1911/90519 |
dc.description.abstract |
Metastasis involves multiple cycles of Epithelial-to-Mesenchymal Transition (EMT) and its reverse-MET. Cells can also undergo partial transitions to attain a hybrid epithelial/mesenchymal (E/M) phenotype that has maximum cellular plasticity and allows migration of Circulating Tumor Cells (CTCs) as a cluster. Hence, deciphering the molecular players helping to maintain the hybrid E/M phenotype may inform anti-metastasis strategies. Here, we devised a mechanism-based mathematical model to couple the transcription factor OVOL with the core EMT regulatory network miR-200/ZEB that acts as a three-way switch between the E, E/M and M phenotypes. We show that OVOL can modulate cellular plasticity in multiple ways - restricting EMT, driving MET, expanding the existence of the hybrid E/M phenotype and turning both EMT and MET into two-step processes. Our theoretical framework explains the differences between the observed effects of OVOL in breast and prostate cancer, and provides a platform for investigating additional signals during metastasis.asis.
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dc.language.iso |
eng
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dc.publisher |
Impact Journals, LLC
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dc.rights |
All content, except where otherwise noted, is licensed under a Creative Commons Attribution 3.0 License.
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dc.rights.uri | http://creativecommons.org/licenses/by/3.0/ |
dc.title |
OVOL guides the epithelial-hybrid-mesenchymal transition
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dc.type |
Journal article
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dc.citation.journalTitle |
Oncotarget
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dc.contributor.org |
Center for Theoretical Biological Physics
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dc.subject.keyword | EMT metastasis OVOL partial EMT cancer systems biology
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dc.citation.volumeNumber |
6
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dc.citation.issueNumber |
17
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dc.type.dcmi |
Text
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dc.identifier.doi | http://dx.doi.org/10.18632/oncotarget.3623 |
dc.identifier.pmcid |
PMC4558162
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dc.identifier.pmid |
25944618
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dc.type.publication |
publisher version
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dc.citation.firstpage |
15436
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dc.citation.lastpage |
15448
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