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Article: miR-200a regulates epithelial-mesenchymal to stem-like transition via ZEB2 and β-catenin signaling
Title | miR-200a regulates epithelial-mesenchymal to stem-like transition via ZEB2 and β-catenin signaling | ||||||
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Authors | |||||||
Issue Date | 2010 | ||||||
Publisher | American 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? | ||||||
Abstract | The 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 Identifier | http://hdl.handle.net/10722/124530 | ||||||
ISSN | 2020 Impact Factor: 5.157 2023 SCImago Journal Rankings: 1.766 | ||||||
PubMed Central ID | |||||||
ISI Accession Number ID |
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 Field | Value | Language |
---|---|---|
dc.contributor.author | Xia, H | en_HK |
dc.contributor.author | Cheung, WKC | en_HK |
dc.contributor.author | Sze, J | en_HK |
dc.contributor.author | Lu, G | en_HK |
dc.contributor.author | Jiang, S | en_HK |
dc.contributor.author | Yao, H | en_HK |
dc.contributor.author | Bian, XW | en_HK |
dc.contributor.author | Poon, WS | en_HK |
dc.contributor.author | Kung, HF | en_HK |
dc.contributor.author | Lin, MC | en_HK |
dc.date.accessioned | 2010-10-31T10:39:41Z | - |
dc.date.available | 2010-10-31T10:39:41Z | - |
dc.date.issued | 2010 | en_HK |
dc.identifier.citation | Journal Of Biological Chemistry, 2010, v. 285 n. 47, p. 36995-37004 | en_HK |
dc.identifier.issn | 0021-9258 | en_HK |
dc.identifier.uri | http://hdl.handle.net/10722/124530 | - |
dc.description.abstract | The 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.language | eng | en_HK |
dc.publisher | American Society for Biochemistry and Molecular Biology, Inc. The Journal's web site is located at http://www.jbc.org/ | en_HK |
dc.relation.ispartof | Journal of Biological Chemistry | en_HK |
dc.rights | Journal of Biological Chemistry. Copyright © American Society for Biochemistry and Molecular Biology, Inc. | - |
dc.subject.mesh | Epithelial-Mesenchymal Transition | - |
dc.subject.mesh | Homeodomain Proteins - antagonists and inhibitors - genetics - metabolism | - |
dc.subject.mesh | MicroRNAs - physiology | - |
dc.subject.mesh | Nasopharyngeal Neoplasms - metabolism - pathology | - |
dc.subject.mesh | Neoplastic Stem Cells - metabolism - pathology | - |
dc.title | miR-200a regulates epithelial-mesenchymal to stem-like transition via ZEB2 and β-catenin signaling | en_HK |
dc.type | Article | en_HK |
dc.identifier.openurl | http://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+signaling | en_HK |
dc.identifier.email | Lin, MC:mcllin@hkucc.hku.hk | en_HK |
dc.identifier.authority | Lin, MC=rp00746 | en_HK |
dc.description.nature | link_to_OA_fulltext | - |
dc.identifier.doi | 10.1074/jbc.M110.133744 | en_HK |
dc.identifier.pmid | 20826811 | - |
dc.identifier.pmcid | PMC2978628 | - |
dc.identifier.scopus | eid_2-s2.0-78449255989 | en_HK |
dc.identifier.hkuros | 181307 | en_HK |
dc.relation.references | http://www.scopus.com/mlt/select.url?eid=2-s2.0-78449255989&selection=ref&src=s&origin=recordpage | en_HK |
dc.identifier.volume | 285 | en_HK |
dc.identifier.issue | 47 | en_HK |
dc.identifier.spage | 36995 | en_HK |
dc.identifier.epage | 37004 | en_HK |
dc.identifier.isi | WOS:000284146100016 | - |
dc.publisher.place | United States | en_HK |
dc.identifier.scopusauthorid | Xia, H=12545165300 | en_HK |
dc.identifier.scopusauthorid | Cheung, WKC=35080070600 | en_HK |
dc.identifier.scopusauthorid | Sze, J=7003867625 | en_HK |
dc.identifier.scopusauthorid | Lu, G=36619108300 | en_HK |
dc.identifier.scopusauthorid | Jiang, S=36523046900 | en_HK |
dc.identifier.scopusauthorid | Yao, H=13104506400 | en_HK |
dc.identifier.scopusauthorid | Bian, XW=7103023096 | en_HK |
dc.identifier.scopusauthorid | Poon, WS=7103025507 | en_HK |
dc.identifier.scopusauthorid | Kung, HF=7402514190 | en_HK |
dc.identifier.scopusauthorid | Lin, MC=7404816359 | en_HK |
dc.identifier.citeulike | 9092501 | - |
dc.identifier.issnl | 0021-9258 | - |