OVOL guides the epithelial-hybrid-mesenchymal transition
dc.citation.firstpage | 15436 | en_US |
dc.citation.issueNumber | 17 | en_US |
dc.citation.journalTitle | Oncotarget | en_US |
dc.citation.lastpage | 15448 | en_US |
dc.citation.volumeNumber | 6 | en_US |
dc.contributor.author | Jia, Dongya | en_US |
dc.contributor.author | Jolly, Mohit Kumar | en_US |
dc.contributor.author | Boareto, Marcelo | en_US |
dc.contributor.author | Parsana, Princy | en_US |
dc.contributor.author | Mooney, Steven M. | en_US |
dc.contributor.author | Pienta, Kenneth J. | en_US |
dc.contributor.author | Levine, Herbert | en_US |
dc.contributor.author | Ben-Jacob, Eshel | en_US |
dc.contributor.org | Center for Theoretical Biological Physics | en_US |
dc.date.accessioned | 2016-06-22T16:28:31Z | en_US |
dc.date.available | 2016-06-22T16:28:31Z | en_US |
dc.date.issued | 2015 | en_US |
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. | en_US |
dc.identifier.citation | Jia, Dongya, Jolly, Mohit Kumar, Boareto, Marcelo, et al.. "OVOL guides the epithelial-hybrid-mesenchymal transition." <i>Oncotarget,</i> 6, no. 17 (2015) Impact Journals, LLC: 15436-15448. http://dx.doi.org/10.18632/oncotarget.3623. | en_US |
dc.identifier.doi | http://dx.doi.org/10.18632/oncotarget.3623 | en_US |
dc.identifier.uri | https://hdl.handle.net/1911/90519 | en_US |
dc.language.iso | eng | en_US |
dc.publisher | Impact Journals, LLC | en_US |
dc.rights | All content, except where otherwise noted, is licensed under a Creative Commons Attribution 3.0 License. | en_US |
dc.rights.uri | http://creativecommons.org/licenses/by/3.0/ | en_US |
dc.subject.keyword | EMT | en_US |
dc.subject.keyword | metastasis | en_US |
dc.subject.keyword | OVOL | en_US |
dc.subject.keyword | partial EMT | en_US |
dc.subject.keyword | cancer systems biology | en_US |
dc.title | OVOL guides the epithelial-hybrid-mesenchymal transition | en_US |
dc.type | Journal article | en_US |
dc.type.dcmi | Text | en_US |
dc.type.publication | publisher version | en_US |
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