LINE-1 couples EMT programming with acquisition of oncogenic phenotypes in human bronchial epithelial cells
Author
Reyes-Reyes, Elsa M.Aispuro, Ivan
Tavera-Garcia, Marco A.
Field, Matthew
Moore, Sara
Ramos, Irma
Ramos, Kenneth S.
Affiliation
Univ Arizona, Coll Med, Div Pulm Allergy Crit Care & Sleep MedUniv Arizona, Canc Ctr
Univ Arizona Hlth Sci, Ctr Appl Genet & Genom Med
Issue Date
2017-10-23
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IMPACT JOURNALS LLCCitation
LINE-1 couples EMT programming with acquisition of oncogenic phenotypes in human bronchial epithelial cells 2017, 8 (61) OncotargetJournal
OncotargetRights
© 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).Collection Information
This 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.Abstract
Although 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.ISSN
1949-2553PubMed ID
29262603Version
Final published versionSponsors
University of Arizona Health Sciences; University of Arizona Diversity and Inclusion Award; Career Development AwardAdditional Links
http://www.oncotarget.com/fulltext/21953ae974a485f413a2113503eed53cd6c53
10.18632/oncotarget.21953
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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).
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