File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: microRNA-146b inhibits glioma cell migration and invasion by targeting MMPs

TitlemicroRNA-146b inhibits glioma cell migration and invasion by targeting MMPs
Authors
KeywordsGlioblastoma
Invasion
Matrix metalloproteinase
Migration
miR-146b
Issue Date2009
PublisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/brainres
Citation
Brain Research, 2009, v. 1269, p. 158-165 How to Cite?
AbstractMicroRNAs (miRNAs) are a class of endogenous, small non-protein coding single-stranded RNA molecules, which are crucial post-transcriptional regulators of gene expression. Previous studies have shown that miRNAs participate in a wide range of biological functions and play important roles in various human diseases including glioma. However, the role of miRNAs in mediating glioblastoma cell migration and invasion has not been elucidated. Using miRNA microarray, we identified miR-146b as one of the miRNAs that is significantly dysregulated in human glioblastoma tissue. We showed that miR-146b overexpression by transfection with the precursor miR-146b, or knock-down by Locked Nucleic Acid (LNA)-modified anti-miR-146b, has no effect on the growth of human glioblastoma U373 cells. However, precursor miR-146b transfection significantly reduced the migration and invasion of U373 cells, while LNA-anti-miR-146b transfection generated the opposite result. Furthermore, we discovered that a matrix metalloproteinase gene, MMP16, is one of the downstream targets of miR-146b. Taken together, our findings suggest that miR-146b is involved in glioma cell migration and invasion by targeting MMPs, and implicate miR-146b as a metastasis-inhibiting miRNA in glioma. © 2008 Elsevier B.V. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/58402
ISSN
2015 Impact Factor: 2.561
2015 SCImago Journal Rankings: 1.351
ISI Accession Number ID
Funding AgencyGrant Number
Key Basic Research Developing Project2007CB947001
2006CB910104
State High Technology Developing2008AA02Z115
Key Programs of National Science Foundation of China30430240
Shanghai Metropolitan Fund for Research and Development04DZ1400S
04JC14096
Foundation of Guangzhou Science and Technology Bureau2005Zl-EO131
Research Grants Council (RGC) of the Hong Kong Special Administrative Region, ChinaCUHK467SO7
HFKHKU7705/07M
Funding Information:

This work was supported by the Key Basic Research Developing Project (2007CB947001, 2006CB910104), State High Technology Developing Project (2008AA02Z115), the Key Programs of National Science Foundation of China (30430240), the Shanghai Metropolitan Fund for Research and Development (04DZ1400S and 04JC14096) and the Foundation of Guangzhou Science and Technology Bureau (2005Zl-EO131), Research Grants Council (RGC) of the Hong Kong Special Administrative Region, China (CUHK467SO7 to HFK; HKU7705/07M to MCL).

References

 

DC FieldValueLanguage
dc.contributor.authorXia, Hen_HK
dc.contributor.authorQi, Yen_HK
dc.contributor.authorNg, SSen_HK
dc.contributor.authorChen, Xen_HK
dc.contributor.authorLi, Den_HK
dc.contributor.authorChen, Sen_HK
dc.contributor.authorGe, Ren_HK
dc.contributor.authorJiang, Sen_HK
dc.contributor.authorLi, Gen_HK
dc.contributor.authorChen, Yen_HK
dc.contributor.authorHe, MLen_HK
dc.contributor.authorKung, Hfen_HK
dc.contributor.authorLai, Len_HK
dc.contributor.authorLin, MCen_HK
dc.date.accessioned2010-05-31T03:29:40Z-
dc.date.available2010-05-31T03:29:40Z-
dc.date.issued2009en_HK
dc.identifier.citationBrain Research, 2009, v. 1269, p. 158-165en_HK
dc.identifier.issn0006-8993en_HK
dc.identifier.urihttp://hdl.handle.net/10722/58402-
dc.description.abstractMicroRNAs (miRNAs) are a class of endogenous, small non-protein coding single-stranded RNA molecules, which are crucial post-transcriptional regulators of gene expression. Previous studies have shown that miRNAs participate in a wide range of biological functions and play important roles in various human diseases including glioma. However, the role of miRNAs in mediating glioblastoma cell migration and invasion has not been elucidated. Using miRNA microarray, we identified miR-146b as one of the miRNAs that is significantly dysregulated in human glioblastoma tissue. We showed that miR-146b overexpression by transfection with the precursor miR-146b, or knock-down by Locked Nucleic Acid (LNA)-modified anti-miR-146b, has no effect on the growth of human glioblastoma U373 cells. However, precursor miR-146b transfection significantly reduced the migration and invasion of U373 cells, while LNA-anti-miR-146b transfection generated the opposite result. Furthermore, we discovered that a matrix metalloproteinase gene, MMP16, is one of the downstream targets of miR-146b. Taken together, our findings suggest that miR-146b is involved in glioma cell migration and invasion by targeting MMPs, and implicate miR-146b as a metastasis-inhibiting miRNA in glioma. © 2008 Elsevier B.V. All rights reserved.en_HK
dc.languageengen_HK
dc.publisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/brainresen_HK
dc.relation.ispartofBrain Researchen_HK
dc.rightsBrain Research. Copyright © Elsevier BV.en_HK
dc.subjectGlioblastomaen_HK
dc.subjectInvasionen_HK
dc.subjectMatrix metalloproteinaseen_HK
dc.subjectMigrationen_HK
dc.subjectmiR-146ben_HK
dc.titlemicroRNA-146b inhibits glioma cell migration and invasion by targeting MMPsen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0006-8993&volume=1269&spage=158&epage=165&date=2009&atitle=microRNA-146b+Inhibits+Glioma+Cell+Migration+and+Invasion+by+Targeting+MMPs+en_HK
dc.identifier.emailNg, SS: ssmng@hku.hken_HK
dc.identifier.emailLin, MC: mcllin@hkucc.hku.hken_HK
dc.identifier.authorityNg, SS=rp00767en_HK
dc.identifier.authorityLin, MC=rp00746en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.brainres.2009.02.037en_HK
dc.identifier.pmid19265686en_HK
dc.identifier.scopuseid_2-s2.0-67349107523en_HK
dc.identifier.hkuros154798en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-67349107523&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume1269en_HK
dc.identifier.spage158en_HK
dc.identifier.epage165en_HK
dc.identifier.isiWOS:000266294900016-
dc.publisher.placeNetherlandsen_HK
dc.identifier.scopusauthoridXia, H=12545165300en_HK
dc.identifier.scopusauthoridQi, Y=24171887800en_HK
dc.identifier.scopusauthoridNg, SS=7403358718en_HK
dc.identifier.scopusauthoridChen, X=24170717900en_HK
dc.identifier.scopusauthoridLi, D=26324923700en_HK
dc.identifier.scopusauthoridChen, S=15757054600en_HK
dc.identifier.scopusauthoridGe, R=7005525090en_HK
dc.identifier.scopusauthoridJiang, S=36523046900en_HK
dc.identifier.scopusauthoridLi, G=7407055832en_HK
dc.identifier.scopusauthoridChen, Y=24075600300en_HK
dc.identifier.scopusauthoridHe, ML=35080389700en_HK
dc.identifier.scopusauthoridKung, Hf=7402514190en_HK
dc.identifier.scopusauthoridLai, L=12445800200en_HK
dc.identifier.scopusauthoridLin, MC=7404816359en_HK

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats