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dc.contributor.authorCai, Yien_US
dc.contributor.authorHirata, Ayakoen_US
dc.contributor.authorNakayama, Soheien_US
dc.contributor.authorVanderLaan, Paul A.en_US
dc.contributor.authorLevantini, Elenaen_US
dc.contributor.authorYamamoto, Mihokoen_US
dc.contributor.authorHirai, Hideyoen_US
dc.contributor.authorWong, Kwok-Kinen_US
dc.contributor.authorCosta, Daniel B.en_US
dc.contributor.authorWatanabe, Hideoen_US
dc.contributor.authorKobayashi, Susumu S.en_US
dc.date.accessioned2015-04-01T15:30:25Z
dc.date.issued2015en_US
dc.identifier.citationCai, Y., A. Hirata, S. Nakayama, P. A. VanderLaan, E. Levantini, M. Yamamoto, H. Hirai, et al. 2015. “CCAAT/Enhancer Binding Protein β Is Dispensable for Development of Lung Adenocarcinoma.” PLoS ONE 10 (3): e0120647. doi:10.1371/journal.pone.0120647. http://dx.doi.org/10.1371/journal.pone.0120647.en
dc.identifier.issn1932-6203en
dc.identifier.urihttp://nrs.harvard.edu/urn-3:HUL.InstRepos:14351287
dc.description.abstractLung cancer is the leading cause of cancer death worldwide. Although disruption of normal proliferation and differentiation is a vital component of tumorigenesis, the mechanisms of this process in lung cancer are still unclear. A transcription factor, C/EBPβ is a critical regulator of proliferation and/or differentiation in multiple tissues. In lung, C/EBPβ is expressed in alveolar pneumocytes and bronchial epithelial cells; however, its roles on normal lung homeostasis and lung cancer development have not been well described. Here we investigated whether C/EBPβ is required for normal lung development and whether its aberrant expression and/or activity contribute to lung tumorigenesis. We showed that C/EBPβ was expressed in both human normal pneumocytes and lung adenocarcinoma cell lines. We found that overall lung architecture was maintained in Cebpb knockout mice. Neither overexpression of nuclear C/EBPβ nor suppression of CEBPB expression had significant effects on cell proliferation. C/EBPβ expression and activity remained unchanged upon EGF stimulation. Furthermore, deletion of Cebpb had no impact on lung tumor burden in a lung specific, conditional mutant EGFR lung cancer mouse model. Analyses of data from The Cancer Genome Atlas (TCGA) revealed that expression, promoter methylation, or copy number of CEBPB was not significantly altered in human lung adenocarcinoma. Taken together, our data suggest that C/EBPβ is dispensable for development of lung adenocarcinoma.en
dc.language.isoen_USen
dc.publisherPublic Library of Scienceen
dc.relation.isversionofdoi:10.1371/journal.pone.0120647en
dc.relation.hasversionhttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC4358974/pdf/en
dash.licenseLAAen_US
dc.titleCCAAT/Enhancer Binding Protein β Is Dispensable for Development of Lung Adenocarcinomaen
dc.typeJournal Articleen_US
dc.description.versionVersion of Recorden
dc.relation.journalPLoS ONEen
dash.depositing.authorNakayama, Soheien_US
dc.date.available2015-04-01T15:30:25Z
dc.identifier.doi10.1371/journal.pone.0120647*
dash.authorsorderedfalse
dash.contributor.affiliatedKobayashi, Susumu
dash.contributor.affiliatedNakayama, Sohei
dash.contributor.affiliatedLevantini, Elena
dash.contributor.affiliatedCosta, Daniel
dash.contributor.affiliatedVanderlaan, Paul


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