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Article: Loss of brain-enriched miR-124 microRNA enhances stem-like traits and invasiveness of glioma cells

TitleLoss of brain-enriched miR-124 microRNA enhances stem-like traits and invasiveness of glioma cells
Authors
Issue Date2012
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, 2012, v. 287 n. 13, p. 9962-9971 How to Cite?
Abstract
miR-124 is a brain-enriched microRNA that plays a crucial role in neural development and has been shown to be down-regulated in glioma and medulloblastoma, suggesting its possible involvement in brain tumor progression. Here, we show that miR-124 is down-regulated in a panel of different grades of glioma tissues and in all of the human glioma cell lines we examined. By integrated bioinformatics analysis and experimental confirmation, we identified SNAI2, which is often up-regulated in glioma, as a direct functional target of miR-124. Because SNAI2 has been shown to regulate stem cell functions, we examined the roles of miR-124 and SNAI2 in glioma cell stem-like traits. The results showed that overexpression of miR-124 and knockdown of SNAI2 reduced neurosphere formation, CD133 + cell subpopulation, and stem cell marker (BMI1, Nanog, and Nestin) expression, and these effects could be rescued by re-expression of SNAI2. Furthermore, enhanced miR-124 expression significantly inhibited glioma cell invasion in vitro. Finally, stable overexpression of miR-124 and knockdown of SNAI2 inhibited the tumorigenicity and invasion of glioma cells in vivo. These findings reveal, for the first time, that the tumor suppressor activity of miR-124 could be partly due to its inhibitory effects on glioma stem-like traits and invasiveness through SNAI2. © 2012 by The American Society for Biochemistry and Molecular Biology, Inc.
Persistent Identifierhttp://hdl.handle.net/10722/146425
ISSN
2013 Impact Factor: 4.600
PubMed Central ID
ISI Accession Number ID
Funding AgencyGrant Number
Research Grants Council of the Hong Kong Special Administrative Region, China467109
470911
National Basic Research Program of China (973 Program)2010CB529400
2010CB912800
Funding Information:

This work was supported by Grants 467109 and 470911 from the Research Grants Council of the Hong Kong Special Administrative Region, China, and by Grants 2010CB529400 and 2010CB912800 from the National Basic Research Program of China (973 Program).

References

 

Author Affiliations
  1. The University of Hong Kong
  2. Sun Yat-Sen University
  3. Southwestern Hospital Chongqing
  4. Yale University School of Medicine
  5. Chinese University of Hong Kong
DC FieldValueLanguage
dc.contributor.authorXia, Hen_HK
dc.contributor.authorCheung, WKCen_HK
dc.contributor.authorNg, SSen_HK
dc.contributor.authorJiang, Xen_HK
dc.contributor.authorJiang, Sen_HK
dc.contributor.authorSze, Jen_HK
dc.contributor.authorLeung, GKKen_HK
dc.contributor.authorLu, Gen_HK
dc.contributor.authorChan, DTMen_HK
dc.contributor.authorBian, XWen_HK
dc.contributor.authorKung, HFen_HK
dc.contributor.authorPoon, WSen_HK
dc.contributor.authorLin, MCen_HK
dc.date.accessioned2012-04-24T07:53:12Z-
dc.date.available2012-04-24T07:53:12Z-
dc.date.issued2012en_HK
dc.identifier.citationJournal Of Biological Chemistry, 2012, v. 287 n. 13, p. 9962-9971en_HK
dc.identifier.issn0021-9258en_HK
dc.identifier.urihttp://hdl.handle.net/10722/146425-
dc.description.abstractmiR-124 is a brain-enriched microRNA that plays a crucial role in neural development and has been shown to be down-regulated in glioma and medulloblastoma, suggesting its possible involvement in brain tumor progression. Here, we show that miR-124 is down-regulated in a panel of different grades of glioma tissues and in all of the human glioma cell lines we examined. By integrated bioinformatics analysis and experimental confirmation, we identified SNAI2, which is often up-regulated in glioma, as a direct functional target of miR-124. Because SNAI2 has been shown to regulate stem cell functions, we examined the roles of miR-124 and SNAI2 in glioma cell stem-like traits. The results showed that overexpression of miR-124 and knockdown of SNAI2 reduced neurosphere formation, CD133 + cell subpopulation, and stem cell marker (BMI1, Nanog, and Nestin) expression, and these effects could be rescued by re-expression of SNAI2. Furthermore, enhanced miR-124 expression significantly inhibited glioma cell invasion in vitro. Finally, stable overexpression of miR-124 and knockdown of SNAI2 inhibited the tumorigenicity and invasion of glioma cells in vivo. These findings reveal, for the first time, that the tumor suppressor activity of miR-124 could be partly due to its inhibitory effects on glioma stem-like traits and invasiveness through SNAI2. © 2012 by The American Society for Biochemistry and Molecular Biology, Inc.en_HK
dc.languageengen_US
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.en_US
dc.subject.meshAntigens, Differentiation - genetics - metabolism-
dc.subject.meshGene Expression Regulation, Neoplastic-
dc.subject.meshGenes, Tumor Suppressor-
dc.subject.meshGlioma - genetics - metabolism - pathology-
dc.subject.meshMicroRNAs - biosynthesis - genetics-
dc.titleLoss of brain-enriched miR-124 microRNA enhances stem-like traits and invasiveness of glioma cellsen_HK
dc.typeArticleen_HK
dc.identifier.emailNg, SS: ssmng@hku.hken_HK
dc.identifier.emailLeung, GKK: gkkleung@hku.hken_HK
dc.identifier.emailLin, MC: mcllin@hkucc.hku.hken_HK
dc.identifier.authorityNg, SS=rp00767en_HK
dc.identifier.authorityLeung, GKK=rp00522en_HK
dc.identifier.authorityLin, MC=rp00746en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1074/jbc.M111.332627en_HK
dc.identifier.pmid22253443en_HK
dc.identifier.pmcidPMC3322968-
dc.identifier.scopuseid_2-s2.0-84858992906en_HK
dc.identifier.hkuros199190en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-84858992906&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume287en_HK
dc.identifier.issue13en_HK
dc.identifier.spage9962en_HK
dc.identifier.epage9971en_HK
dc.identifier.isiWOS:000302167200028-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridXia, H=12545165300en_HK
dc.identifier.scopusauthoridCheung, WKC=35080070600en_HK
dc.identifier.scopusauthoridNg, SS=7403358718en_HK
dc.identifier.scopusauthoridJiang, X=55142274600en_HK
dc.identifier.scopusauthoridJiang, S=36523046900en_HK
dc.identifier.scopusauthoridSze, J=7003867625en_HK
dc.identifier.scopusauthoridLeung, GKK=35965118200en_HK
dc.identifier.scopusauthoridLu, G=36619108300en_HK
dc.identifier.scopusauthoridChan, DTM=7402216549en_HK
dc.identifier.scopusauthoridBian, XW=7103023096en_HK
dc.identifier.scopusauthoridKung, HF=7402514190en_HK
dc.identifier.scopusauthoridPoon, WS=7103025507en_HK
dc.identifier.scopusauthoridLin, MC=7404816359en_HK

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