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LINE-1 couples EMT programming with acquisition of oncogenic phenotypes in human bronchial epithelial cells

dc.contributor.authorReyes-Reyes, Elsa M.
dc.contributor.authorAispuro, Ivan
dc.contributor.authorTavera-Garcia, Marco A.
dc.contributor.authorField, Matthew
dc.contributor.authorMoore, Sara
dc.contributor.authorRamos, Irma
dc.contributor.authorRamos, Kenneth S.
dc.date.accessioned2018-03-15T23:19:00Z
dc.date.available2018-03-15T23:19:00Z
dc.date.issued2017-10-23
dc.identifier.citationLINE-1 couples EMT programming with acquisition of oncogenic phenotypes in human bronchial epithelial cells 2017, 8 (61) Oncotargeten
dc.identifier.issn1949-2553
dc.identifier.pmid29262603
dc.identifier.doi10.18632/oncotarget.21953
dc.identifier.urihttp://hdl.handle.net/10150/627063
dc.description.abstractAlthough several lines of evidence have established the central role of epithelial-to-mesenchymal-transition (EMT) in malignant progression of non-small cell lung cancers (NSCLCs), the molecular events connecting EMT to malignancy remain poorly understood. This study presents evidence that Long Interspersed Nuclear Element-1 (LINE-1) retrotransposon couples EMT programming with malignancy in human bronchial epithelial cells (BEAS-2B). This conclusion is supported by studies showing that: 1) activation of EMT programming by TGF-beta 1 increases LINE-1 mRNAs and protein; 2) the lung carcinogen benzo(a)pyrene coregulates TGF-beta 1 and LINE-1 mRNAs, with LINE-1 positioned downstream of TGF-beta 1 signaling; and, 3) forced expression of LINE-1 in BEAS-2B cells recapitulates EMT programming and induces malignant phenotypes and tumorigenesis in vivo. These findings identify a TGF beta 1-LINE-1 axis as a critical effector pathway that can be targeted for the development of precision therapies during malignant progression of intractable NSCLCs.
dc.description.sponsorshipUniversity of Arizona Health Sciences; University of Arizona Diversity and Inclusion Award; Career Development Awarden
dc.language.isoenen
dc.publisherIMPACT JOURNALS LLCen
dc.relation.urlhttp://www.oncotarget.com/fulltext/21953en
dc.rights© Reyes-Reyes et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License 3.0 (CC BY 3.0).en
dc.rights.urihttps://creativecommons.org/licenses/by/3.0/
dc.subjectLINE-1en
dc.subjectEMT programmingen
dc.subjectoncogenesisen
dc.titleLINE-1 couples EMT programming with acquisition of oncogenic phenotypes in human bronchial epithelial cellsen
dc.typeArticleen
dc.contributor.departmentUniv Arizona, Coll Med, Div Pulm Allergy Crit Care & Sleep Meden
dc.contributor.departmentUniv Arizona, Canc Ctren
dc.contributor.departmentUniv Arizona Hlth Sci, Ctr Appl Genet & Genom Meden
dc.identifier.journalOncotargeten
dc.description.collectioninformationThis item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at repository@u.library.arizona.edu.en
dc.eprint.versionFinal published versionen
refterms.dateFOA2018-06-17T11:28:43Z
html.description.abstractAlthough several lines of evidence have established the central role of epithelial-to-mesenchymal-transition (EMT) in malignant progression of non-small cell lung cancers (NSCLCs), the molecular events connecting EMT to malignancy remain poorly understood. This study presents evidence that Long Interspersed Nuclear Element-1 (LINE-1) retrotransposon couples EMT programming with malignancy in human bronchial epithelial cells (BEAS-2B). This conclusion is supported by studies showing that: 1) activation of EMT programming by TGF-beta 1 increases LINE-1 mRNAs and protein; 2) the lung carcinogen benzo(a)pyrene coregulates TGF-beta 1 and LINE-1 mRNAs, with LINE-1 positioned downstream of TGF-beta 1 signaling; and, 3) forced expression of LINE-1 in BEAS-2B cells recapitulates EMT programming and induces malignant phenotypes and tumorigenesis in vivo. These findings identify a TGF beta 1-LINE-1 axis as a critical effector pathway that can be targeted for the development of precision therapies during malignant progression of intractable NSCLCs.


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© Reyes-Reyes et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License 3.0 (CC BY 3.0).
Except where otherwise noted, this item's license is described as © Reyes-Reyes et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License 3.0 (CC BY 3.0).