File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Runx3 is a crucial regulator of alveolar differentiation and lung tumorigenesis in mice

TitleRunx3 is a crucial regulator of alveolar differentiation and lung tumorigenesis in mice
Authors
Issue Date2011
PublisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/DIF
Citation
Differentiation, 2011, v. 81 n. 4, p. 261-268 How to Cite?
AbstractThe runt-domain transcription factor Runx3 plays crucial roles during development such as regulating gene expression. It has been shown that Runx3 is involved in neurogenesis, thymopoiesis and functions like a tumor suppressor. Runx3 null mouse die soon after birth as a result of multiple organ defects. Runx3 null mouse lung shows an abnormal phenotype and loss of Runx3 induced remodeling in the lung. Interestingly, lung adenocarcinoma is observed in Runx3 heterozygous mice at 18 months of age. During lung development various cellular and molecular events occur such as cell proliferation, cell death, differentiation and epithelial-mesenchymal transition (EMT). To understand the specific lethal events in Runx3 null mice, we examined cellular and molecular networks involved in EMT, and EMT inducers were quantified by RT-qPCR during lung development. Excessive EMT was observed in lungs at PN1 day in Runx3 null mice and PN18 months in Runx3 heterozygous mice. Pharmacologic inhibition of EMT was used to curb tumor progression. In this study, U0126 was injected to pregnant mouse for inhibition of pERK signaling. After U0126 treatment, life spans of newborn mice were increased and lung hyperplasia was partially rescued by down-regulated cell proliferation and EMT. Our data suggest that Runx3 is involved in crucial regulation of alveolar differentiation and tumor suppression in developing mouse lung. © 2011 International Society of Differentiation.
Persistent Identifierhttp://hdl.handle.net/10722/169579
ISSN
2015 Impact Factor: 2.461
2015 SCImago Journal Rankings: 1.747
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLee, JMen_US
dc.contributor.authorShin, JOen_US
dc.contributor.authorCho, KWen_US
dc.contributor.authorHosoya, Aen_US
dc.contributor.authorCho, SWen_US
dc.contributor.authorLee, YSen_US
dc.contributor.authorRyoo, HMen_US
dc.contributor.authorBae, SCen_US
dc.contributor.authorJung, HSen_US
dc.date.accessioned2012-10-25T04:53:05Z-
dc.date.available2012-10-25T04:53:05Z-
dc.date.issued2011en_US
dc.identifier.citationDifferentiation, 2011, v. 81 n. 4, p. 261-268en_US
dc.identifier.issn0301-4681en_US
dc.identifier.urihttp://hdl.handle.net/10722/169579-
dc.description.abstractThe runt-domain transcription factor Runx3 plays crucial roles during development such as regulating gene expression. It has been shown that Runx3 is involved in neurogenesis, thymopoiesis and functions like a tumor suppressor. Runx3 null mouse die soon after birth as a result of multiple organ defects. Runx3 null mouse lung shows an abnormal phenotype and loss of Runx3 induced remodeling in the lung. Interestingly, lung adenocarcinoma is observed in Runx3 heterozygous mice at 18 months of age. During lung development various cellular and molecular events occur such as cell proliferation, cell death, differentiation and epithelial-mesenchymal transition (EMT). To understand the specific lethal events in Runx3 null mice, we examined cellular and molecular networks involved in EMT, and EMT inducers were quantified by RT-qPCR during lung development. Excessive EMT was observed in lungs at PN1 day in Runx3 null mice and PN18 months in Runx3 heterozygous mice. Pharmacologic inhibition of EMT was used to curb tumor progression. In this study, U0126 was injected to pregnant mouse for inhibition of pERK signaling. After U0126 treatment, life spans of newborn mice were increased and lung hyperplasia was partially rescued by down-regulated cell proliferation and EMT. Our data suggest that Runx3 is involved in crucial regulation of alveolar differentiation and tumor suppression in developing mouse lung. © 2011 International Society of Differentiation.en_US
dc.languageengen_US
dc.publisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/DIFen_US
dc.relation.ispartofDifferentiationen_US
dc.subject.meshAdenocarcinoma - Geneticsen_US
dc.subject.meshAnimalsen_US
dc.subject.meshButadienes - Pharmacologyen_US
dc.subject.meshCell Differentiation - Geneticsen_US
dc.subject.meshCell Transformation, Neoplastic - Geneticsen_US
dc.subject.meshCore Binding Factor Alpha 3 Subunit - Genetics - Physiologyen_US
dc.subject.meshEpithelial-Mesenchymal Transition - Drug Effects - Geneticsen_US
dc.subject.meshFemaleen_US
dc.subject.meshGene Expression Regulation, Developmentalen_US
dc.subject.meshLung - Abnormalities - Growth & Development - Metabolismen_US
dc.subject.meshLung Neoplasms - Geneticsen_US
dc.subject.meshMiceen_US
dc.subject.meshMice, Knockouten_US
dc.subject.meshNitriles - Pharmacologyen_US
dc.subject.meshPregnancyen_US
dc.subject.meshPulmonary Alveoli - Growth & Development - Metabolismen_US
dc.subject.meshSignal Transductionen_US
dc.subject.meshEif-2 Kinase - Antagonists & Inhibitors - Geneticsen_US
dc.titleRunx3 is a crucial regulator of alveolar differentiation and lung tumorigenesis in miceen_US
dc.typeArticleen_US
dc.identifier.emailJung, HS: hsjung@yuhs.acen_US
dc.identifier.authorityJung, HS=rp01683en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/j.diff.2011.02.001en_US
dc.identifier.pmid21367515-
dc.identifier.scopuseid_2-s2.0-79954570409en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-79954570409&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume81en_US
dc.identifier.issue4en_US
dc.identifier.spage261en_US
dc.identifier.epage268en_US
dc.identifier.isiWOS:000289557900007-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridLee, JM=41361401200en_US
dc.identifier.scopusauthoridShin, JO=37361704500en_US
dc.identifier.scopusauthoridCho, KW=7403956665en_US
dc.identifier.scopusauthoridHosoya, A=8651007100en_US
dc.identifier.scopusauthoridCho, SW=32967447200en_US
dc.identifier.scopusauthoridLee, YS=48061093000en_US
dc.identifier.scopusauthoridRyoo, HM=7005485966en_US
dc.identifier.scopusauthoridBae, SC=7202714699en_US
dc.identifier.scopusauthoridJung, HS=7403030195en_US

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats