File Download
  Links for fulltext
     (May Require Subscription)
Supplementary

Article: miR-200a regulates epithelial-mesenchymal to stem-like transition via ZEB2 and β-catenin signaling

TitlemiR-200a regulates epithelial-mesenchymal to stem-like transition via ZEB2 and β-catenin signaling
Authors
Issue Date2010
PublisherAmerican Society for Biochemistry and Molecular Biology, Inc. The Journal's web site is located at http://www.jbc.org/
Citation
Journal Of Biological Chemistry, 2010, v. 285 n. 47, p. 36995-37004 How to Cite?
AbstractThe emerging concept of generating cancer stem cells from epithelial-mesenchymal transition has attracted great interest; however, the factors and molecular mechanisms that govern this putative tumor-initiating process remain largely elusive. We report here that miR-200a not only regulates epithelial-mesenchymal transition but also stem-like transition in nasopharyngeal carcinoma cells. We first showed that stable knockdown of miR-200a promotes the transition of epithelium-like CNE-1 cells to the mesenchymal phenotype. More importantly, it also induced several stem cell-like traits, including CD133 + side population, sphere formation capacity, in vivo tumorigenicity in nude mice, and stem cell marker expression. Consistently, stable overexpression of miR-200a switched mesenchyme-like C666-1 cells to the epithelial state, accompanied by a significant reduction of stem-like cell features. Furthermore, in vitro differentiation of the C666-1 tumor sphere resulted in diminished stem-like cell population and miR-200a induction. To investigate the molecular mechanism, we demonstrated that miR-200a controls epithelial-mesenchymal transition by targeting ZEB2, although it regulates the stem-like transition differentially and specifically by β-catenin signaling. Our findings reveal for the first time the function of miR-200a in shifting nasopharyngeal carcinoma cell states via a reversible process coined as epithelial-mesenchymal to stem-like transition through differential and specific mechanisms. © 2010 by The American Society for Biochemistry and Molecular Biology, Inc.
Persistent Identifierhttp://hdl.handle.net/10722/124530
ISSN
2015 Impact Factor: 4.258
2015 SCImago Journal Rankings: 3.151
PubMed Central ID
ISI Accession Number ID
Funding AgencyGrant Number
Research Grants Council of Hong Kong467109
National Basic Research Program of China (973 Program)2010CB529400
2010CB912800
Funding Information:

This work was supported by Research Grants Council of Hong Kong Grant 467109 and National Basic Research Program of China (973 Program) Grants 2010CB529400 and 2010CB912800.

References

 

DC FieldValueLanguage
dc.contributor.authorXia, Hen_HK
dc.contributor.authorCheung, WKCen_HK
dc.contributor.authorSze, Jen_HK
dc.contributor.authorLu, Gen_HK
dc.contributor.authorJiang, Sen_HK
dc.contributor.authorYao, Hen_HK
dc.contributor.authorBian, XWen_HK
dc.contributor.authorPoon, WSen_HK
dc.contributor.authorKung, HFen_HK
dc.contributor.authorLin, MCen_HK
dc.date.accessioned2010-10-31T10:39:41Z-
dc.date.available2010-10-31T10:39:41Z-
dc.date.issued2010en_HK
dc.identifier.citationJournal Of Biological Chemistry, 2010, v. 285 n. 47, p. 36995-37004en_HK
dc.identifier.issn0021-9258en_HK
dc.identifier.urihttp://hdl.handle.net/10722/124530-
dc.description.abstractThe emerging concept of generating cancer stem cells from epithelial-mesenchymal transition has attracted great interest; however, the factors and molecular mechanisms that govern this putative tumor-initiating process remain largely elusive. We report here that miR-200a not only regulates epithelial-mesenchymal transition but also stem-like transition in nasopharyngeal carcinoma cells. We first showed that stable knockdown of miR-200a promotes the transition of epithelium-like CNE-1 cells to the mesenchymal phenotype. More importantly, it also induced several stem cell-like traits, including CD133 + side population, sphere formation capacity, in vivo tumorigenicity in nude mice, and stem cell marker expression. Consistently, stable overexpression of miR-200a switched mesenchyme-like C666-1 cells to the epithelial state, accompanied by a significant reduction of stem-like cell features. Furthermore, in vitro differentiation of the C666-1 tumor sphere resulted in diminished stem-like cell population and miR-200a induction. To investigate the molecular mechanism, we demonstrated that miR-200a controls epithelial-mesenchymal transition by targeting ZEB2, although it regulates the stem-like transition differentially and specifically by β-catenin signaling. Our findings reveal for the first time the function of miR-200a in shifting nasopharyngeal carcinoma cell states via a reversible process coined as epithelial-mesenchymal to stem-like transition through differential and specific mechanisms. © 2010 by The American Society for Biochemistry and Molecular Biology, Inc.en_HK
dc.languageengen_HK
dc.publisherAmerican Society for Biochemistry and Molecular Biology, Inc. The Journal's web site is located at http://www.jbc.org/en_HK
dc.relation.ispartofJournal of Biological Chemistryen_HK
dc.rightsJournal of Biological Chemistry. Copyright © American Society for Biochemistry and Molecular Biology, Inc.-
dc.subject.meshEpithelial-Mesenchymal Transition-
dc.subject.meshHomeodomain Proteins - antagonists and inhibitors - genetics - metabolism-
dc.subject.meshMicroRNAs - physiology-
dc.subject.meshNasopharyngeal Neoplasms - metabolism - pathology-
dc.subject.meshNeoplastic Stem Cells - metabolism - pathology-
dc.titlemiR-200a regulates epithelial-mesenchymal to stem-like transition via ZEB2 and β-catenin signalingen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0021-9258&volume=285&issue=47&spage=36995&epage=37004&date=2010&atitle=miR-200a+regulates+epithelial-mesenchymal+to+stem-like+transition+via+ZEB2+and+beta-catenin+signalingen_HK
dc.identifier.emailLin, MC:mcllin@hkucc.hku.hken_HK
dc.identifier.authorityLin, MC=rp00746en_HK
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1074/jbc.M110.133744en_HK
dc.identifier.pmid20826811-
dc.identifier.pmcidPMC2978628-
dc.identifier.scopuseid_2-s2.0-78449255989en_HK
dc.identifier.hkuros181307en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-78449255989&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume285en_HK
dc.identifier.issue47en_HK
dc.identifier.spage36995en_HK
dc.identifier.epage37004en_HK
dc.identifier.isiWOS:000284146100016-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridXia, H=12545165300en_HK
dc.identifier.scopusauthoridCheung, WKC=35080070600en_HK
dc.identifier.scopusauthoridSze, J=7003867625en_HK
dc.identifier.scopusauthoridLu, G=36619108300en_HK
dc.identifier.scopusauthoridJiang, S=36523046900en_HK
dc.identifier.scopusauthoridYao, H=13104506400en_HK
dc.identifier.scopusauthoridBian, XW=7103023096en_HK
dc.identifier.scopusauthoridPoon, WS=7103025507en_HK
dc.identifier.scopusauthoridKung, HF=7402514190en_HK
dc.identifier.scopusauthoridLin, MC=7404816359en_HK
dc.identifier.citeulike9092501-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats