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Article: Mesenchymal stromal cells may enhance metastasis of neuroblastoma via SDF-1/CXCR4 and SDF-1/CXCR7 signaling

TitleMesenchymal stromal cells may enhance metastasis of neuroblastoma via SDF-1/CXCR4 and SDF-1/CXCR7 signaling
Authors
Ma, MYe, JYDeng, RDee, CMChan, GCF
KeywordsCXCR4
CXCR7
MSCs
Neuroblastoma
SDF-1
Issue Date2011
PublisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/canlet
Citation
Cancer Letters, 2011, v. 312 n. 1, p. 1-10 How to Cite?
DOI: http://dx.doi.org/10.1016/j.canlet.2011.06.028
AbstractBone marrow metastasis is frequently observed in patients with high-risk neuroblastoma. Mesenchymal stromal cells (MSCs) in bone marrow may enhance tumor metastasis through secreting stromal cell-derived factor-1 (SDF-1). Here we investigated neuroblastoma cell behaviors under the influence of MSCs and explored the function of SDF-1 signaling during metastasis. Neuroblastoma expressed both of the SDF-1 receptors CXCR4 and CXCR7 shRNA knockdown showed that these receptors were responsible for the migration of neuroblastoma towards MSCs. CXCR4 also supported neuroblastoma invasion. These effects could be effectively blocked by AMD3100, a potent SDF-1 antagonist. Our study suggests that MSCs are important for neuroblastoma metastasis via the secretion of SDF-1 and that such effect can be inhibited by AMD3100 or shRNA knockdown. © 2011 Elsevier Ireland Ltd.
Persistent Identifierhttp://hdl.handle.net/10722/137478
ISSN
0304-3835
2021 Impact Factor: 9.756
2020 SCImago Journal Rankings: 2.470
ISI Accession Number ID
WOS:000296164900001
Funding AgencyGrant Number
Hotung SK Fund
CRCG
HKU
Funding Information:

We sincerely acknowledge the technical assistance from Mr. Chi Shing Leung and Mr. Shing Chan. We also thank Mr. Ka Wai Cheung and Mr. Chow Yee Lai for valuable discussion. This study was supported by Hotung SK Fund, CRCG Grant and HKU postgraduate studentship.

References
References in Scopus

 

DC FieldValueLanguage
dc.contributor.authorMa, Men_HK
dc.contributor.authorYe, JYen_HK
dc.contributor.authorDeng, Ren_HK
dc.contributor.authorDee, CMen_HK
dc.contributor.authorChan, GCFen_HK
dc.date.accessioned2011-08-26T14:25:51Z-
dc.date.available2011-08-26T14:25:51Z-
dc.date.issued2011en_HK
dc.identifier.citationCancer Letters, 2011, v. 312 n. 1, p. 1-10en_HK
dc.identifier.issn0304-3835en_HK
dc.identifier.urihttp://hdl.handle.net/10722/137478-
dc.description.abstractBone marrow metastasis is frequently observed in patients with high-risk neuroblastoma. Mesenchymal stromal cells (MSCs) in bone marrow may enhance tumor metastasis through secreting stromal cell-derived factor-1 (SDF-1). Here we investigated neuroblastoma cell behaviors under the influence of MSCs and explored the function of SDF-1 signaling during metastasis. Neuroblastoma expressed both of the SDF-1 receptors CXCR4 and CXCR7 shRNA knockdown showed that these receptors were responsible for the migration of neuroblastoma towards MSCs. CXCR4 also supported neuroblastoma invasion. These effects could be effectively blocked by AMD3100, a potent SDF-1 antagonist. Our study suggests that MSCs are important for neuroblastoma metastasis via the secretion of SDF-1 and that such effect can be inhibited by AMD3100 or shRNA knockdown. © 2011 Elsevier Ireland Ltd.en_HK
dc.languageengen_US
dc.publisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/canleten_HK
dc.relation.ispartofCancer Lettersen_HK
dc.subjectCXCR4en_HK
dc.subjectCXCR7en_HK
dc.subjectMSCsen_HK
dc.subjectNeuroblastomaen_HK
dc.subjectSDF-1en_HK
dc.titleMesenchymal stromal cells may enhance metastasis of neuroblastoma via SDF-1/CXCR4 and SDF-1/CXCR7 signalingen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0304-3835&volume=312&issue=1&spage=1&epage=10&date=2011&atitle=Mesenchymal+stromal+cells+may+enhance+metastasis+of+neuroblastoma+via+SDF-1/CXCR4+and+SDF-1/CXCR7+signalingen_US
dc.identifier.emailChan, GCF:gcfchan@hkucc.hku.hken_HK
dc.identifier.authorityChan, GCF=rp00431en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.canlet.2011.06.028en_HK
dc.identifier.pmid21906874-
dc.identifier.scopuseid_2-s2.0-80053335731en_HK
dc.identifier.hkuros191926en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-80053335731&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume312en_HK
dc.identifier.issue1en_HK
dc.identifier.spage1en_HK
dc.identifier.epage10en_HK
dc.identifier.eissn1872-7980-
dc.identifier.isiWOS:000296164900001-
dc.publisher.placeIrelanden_HK
dc.identifier.scopusauthoridMa, M=37073032200en_HK
dc.identifier.scopusauthoridYe, JY=23669624100en_HK
dc.identifier.scopusauthoridDeng, R=35209695100en_HK
dc.identifier.scopusauthoridDee, CM=53867760200en_HK
dc.identifier.scopusauthoridChan, GCF=16160154400en_HK
dc.identifier.citeulike9651727-
dc.identifier.issnl0304-3835-

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