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Article: Loss of brain-enriched miR-124 microRNA enhances stem-like traits and invasiveness of glioma cells
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TitleLoss of brain-enriched miR-124 microRNA enhances stem-like traits and invasiveness of glioma cells
 
AuthorsXia, H5 1 2
Cheung, WKC1 4
Ng, SS1
Jiang, X2
Jiang, S2
Sze, J5 1
Leung, GKK1
Lu, G5
Chan, DTM5
Bian, XW3
Kung, HF5 3
Poon, WS5
Lin, MC5 3 1
 
Issue Date2012
 
PublisherAmerican Society for Biochemistry and Molecular Biology, Inc. The Journal's web site is located at http://www.jbc.org/
 
CitationJournal Of Biological Chemistry, 2012, v. 287 n. 13, p. 9962-9971 [How to Cite?]
DOI: http://dx.doi.org/10.1074/jbc.M111.332627
 
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.
 
ISSN0021-9258
2013 Impact Factor: 4.600
 
DOIhttp://dx.doi.org/10.1074/jbc.M111.332627
 
PubMed Central IDPMC3322968
 
ISI Accession Number IDWOS:000302167200028
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).

 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorXia, H
 
dc.contributor.authorCheung, WKC
 
dc.contributor.authorNg, SS
 
dc.contributor.authorJiang, X
 
dc.contributor.authorJiang, S
 
dc.contributor.authorSze, J
 
dc.contributor.authorLeung, GKK
 
dc.contributor.authorLu, G
 
dc.contributor.authorChan, DTM
 
dc.contributor.authorBian, XW
 
dc.contributor.authorKung, HF
 
dc.contributor.authorPoon, WS
 
dc.contributor.authorLin, MC
 
dc.date.accessioned2012-04-24T07:53:12Z
 
dc.date.available2012-04-24T07:53:12Z
 
dc.date.issued2012
 
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.
 
dc.description.natureLink_to_subscribed_fulltext
 
dc.identifier.citationJournal Of Biological Chemistry, 2012, v. 287 n. 13, p. 9962-9971 [How to Cite?]
DOI: http://dx.doi.org/10.1074/jbc.M111.332627
 
dc.identifier.doihttp://dx.doi.org/10.1074/jbc.M111.332627
 
dc.identifier.epage9971
 
dc.identifier.hkuros199190
 
dc.identifier.isiWOS:000302167200028
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).

 
dc.identifier.issn0021-9258
2013 Impact Factor: 4.600
 
dc.identifier.issue13
 
dc.identifier.pmcidPMC3322968
 
dc.identifier.pmid22253443
 
dc.identifier.scopuseid_2-s2.0-84858992906
 
dc.identifier.spage9962
 
dc.identifier.urihttp://hdl.handle.net/10722/146425
 
dc.identifier.volume287
 
dc.languageeng
 
dc.publisherAmerican Society for Biochemistry and Molecular Biology, Inc. The Journal's web site is located at http://www.jbc.org/
 
dc.publisher.placeUnited States
 
dc.relation.ispartofJournal of Biological Chemistry
 
dc.relation.referencesReferences in Scopus
 
dc.rightsJournal of Biological Chemistry. Copyright © American Society for Biochemistry and Molecular Biology, Inc.
 
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 cells
 
dc.typeArticle
 
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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