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Article: The chemokine CXCL12 and its receptor CXCR4 promote glioma stem cell-mediated VEGF production and tumour angiogenesis via PI3K/AKT signalling

TitleThe chemokine CXCL12 and its receptor CXCR4 promote glioma stem cell-mediated VEGF production and tumour angiogenesis via PI3K/AKT signalling
Authors
Issue Date2011
PublisherJohn Wiley & Sons. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/1130
Citation
Journal Of Pathology, 2011, v. 224 n. 3, p. 344-354 How to Cite?
AbstractChemokines and their receptors are actively involved in inflammation, immune responses, and cancer development. Here we report the detection of CD133 + glioma stem-like cells (GSCs) co-expressing a chemokine receptor CXCR4 in human primary glioma tissues. These GSCs were located in areas adjacent to tumour vascular capillaries, suggesting an association between GSCs and tumour angiogenesis. To test this hypothesis, we isolated CD133 + GSCs from surgical specimens of human primary gliomas and glioma cell lines. As compared to CD133 - cells, CD133 + GSCs expressed significantly higher levels of CXCR4 mRNA and protein, and migrated more efficiently in response to the CXCR4 ligand CXCL12. In addition, CXCL12 induced vascular endothelial growth factor (VEGF) production by CD133 + GSCs via activation of the PI3K/AKT signalling pathway. Furthermore, knocking down of CXCR4 using RNA interference or inhibition of CXCR4 function by an antagonist AMD3100 not only reduced VEGF production by CD133 + GSCs in vitro, but also attenuated the growth and angiogenesis of tumour xenografts in vivo formed by CD133 + GSCs in SCID mice. These results indicate that CXCL12 and its receptor CXCR4 promote GSC-initiated glioma growth and angiogenesis by stimulating VEGF production. Copyright © 2011 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
Persistent Identifierhttp://hdl.handle.net/10722/168533
ISSN
2015 Impact Factor: 7.381
2015 SCImago Journal Rankings: 4.176
References

 

DC FieldValueLanguage
dc.contributor.authorPing, YFen_US
dc.contributor.authorYao, XHen_US
dc.contributor.authorJiang, JYen_US
dc.contributor.authorZhao, LTen_US
dc.contributor.authorYu, SCen_US
dc.contributor.authorJiang, Ten_US
dc.contributor.authorLin, MCMen_US
dc.contributor.authorChen, JHen_US
dc.contributor.authorWang, Ben_US
dc.contributor.authorZhang, Ren_US
dc.contributor.authorCui, YHen_US
dc.contributor.authorQian, Cen_US
dc.contributor.authorWang, JMen_US
dc.contributor.authorBian, XWen_US
dc.date.accessioned2012-10-08T03:20:12Z-
dc.date.available2012-10-08T03:20:12Z-
dc.date.issued2011en_US
dc.identifier.citationJournal Of Pathology, 2011, v. 224 n. 3, p. 344-354en_US
dc.identifier.issn0022-3417en_US
dc.identifier.urihttp://hdl.handle.net/10722/168533-
dc.description.abstractChemokines and their receptors are actively involved in inflammation, immune responses, and cancer development. Here we report the detection of CD133 + glioma stem-like cells (GSCs) co-expressing a chemokine receptor CXCR4 in human primary glioma tissues. These GSCs were located in areas adjacent to tumour vascular capillaries, suggesting an association between GSCs and tumour angiogenesis. To test this hypothesis, we isolated CD133 + GSCs from surgical specimens of human primary gliomas and glioma cell lines. As compared to CD133 - cells, CD133 + GSCs expressed significantly higher levels of CXCR4 mRNA and protein, and migrated more efficiently in response to the CXCR4 ligand CXCL12. In addition, CXCL12 induced vascular endothelial growth factor (VEGF) production by CD133 + GSCs via activation of the PI3K/AKT signalling pathway. Furthermore, knocking down of CXCR4 using RNA interference or inhibition of CXCR4 function by an antagonist AMD3100 not only reduced VEGF production by CD133 + GSCs in vitro, but also attenuated the growth and angiogenesis of tumour xenografts in vivo formed by CD133 + GSCs in SCID mice. These results indicate that CXCL12 and its receptor CXCR4 promote GSC-initiated glioma growth and angiogenesis by stimulating VEGF production. Copyright © 2011 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.en_US
dc.languageengen_US
dc.publisherJohn Wiley & Sons. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/1130en_US
dc.relation.ispartofJournal of Pathologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshAntigens, Cd - Metabolismen_US
dc.subject.meshAntigens, Cd31 - Metabolismen_US
dc.subject.meshCell Transformation, Neoplastic - Genetics - Pathologyen_US
dc.subject.meshChemokine Cxcl12 - Physiologyen_US
dc.subject.meshGene Knockdown Techniquesen_US
dc.subject.meshGlioma - Blood Supply - Drug Therapy - Metabolism - Pathologyen_US
dc.subject.meshGlycoproteins - Metabolismen_US
dc.subject.meshHeterocyclic Compounds - Pharmacology - Therapeutic Useen_US
dc.subject.meshHumansen_US
dc.subject.meshMiceen_US
dc.subject.meshMice, Sciden_US
dc.subject.meshNeoplasm Proteins - Metabolism - Physiologyen_US
dc.subject.meshNeoplastic Stem Cells - Drug Effects - Metabolism - Pathologyen_US
dc.subject.meshNeovascularization, Pathologic - Drug Therapy - Metabolism - Pathologyen_US
dc.subject.meshPeptides - Metabolismen_US
dc.subject.meshPhosphatidylinositol 3-Kinases - Physiologyen_US
dc.subject.meshRna, Small Interfering - Geneticsen_US
dc.subject.meshReceptors, Cxcr4 - Antagonists & Inhibitors - Genetics - Physiologyen_US
dc.subject.meshSignal Transduction - Physiologyen_US
dc.subject.meshTumor Stem Cell Assayen_US
dc.subject.meshVascular Endothelial Growth Factor A - Biosynthesisen_US
dc.subject.meshXenograft Model Antitumor Assaysen_US
dc.titleThe chemokine CXCL12 and its receptor CXCR4 promote glioma stem cell-mediated VEGF production and tumour angiogenesis via PI3K/AKT signallingen_US
dc.typeArticleen_US
dc.identifier.emailLin, MCM:mcllin@hkucc.hku.hken_US
dc.identifier.authorityLin, MCM=rp00746en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1002/path.2908en_US
dc.identifier.pmid21618540-
dc.identifier.scopuseid_2-s2.0-79958189212en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-79958189212&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume224en_US
dc.identifier.issue3en_US
dc.identifier.spage344en_US
dc.identifier.epage354en_US
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridPing, YF=16242526900en_US
dc.identifier.scopusauthoridYao, XH=12780653100en_US
dc.identifier.scopusauthoridJiang, JY=36113734200en_US
dc.identifier.scopusauthoridZhao, LT=36116364700en_US
dc.identifier.scopusauthoridYu, SC=25629204700en_US
dc.identifier.scopusauthoridJiang, T=26428206600en_US
dc.identifier.scopusauthoridLin, MCM=7404816359en_US
dc.identifier.scopusauthoridChen, JH=49960897500en_US
dc.identifier.scopusauthoridWang, B=49962706200en_US
dc.identifier.scopusauthoridZhang, R=35498428600en_US
dc.identifier.scopusauthoridCui, YH=54790519600en_US
dc.identifier.scopusauthoridQian, C=7202311152en_US
dc.identifier.scopusauthoridWang, JM=7409528905en_US
dc.identifier.scopusauthoridBian, XW=7103023096en_US

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