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Article: Implications of endocrine gland - Derived vascular endothelial growth factor/prokineticin-1 signaling in human neuroblastoma progression

TitleImplications of endocrine gland - Derived vascular endothelial growth factor/prokineticin-1 signaling in human neuroblastoma progression
Authors
Issue Date2007
PublisherAmerican Association for Cancer Research
Citation
Clinical Cancer Research, 2007, v. 13 n. 3, p. 868-875 How to Cite?
AbstractPurpose: Neuroblastoma is a common pediatric tumor that is derived from improperly differentiated neural crest cells (NCC). We recently revealed that endocrine gland - derived vascular endothelial growth factor/prokineticin-1 (EG-VEGF/Prok-1) is a key factor mediating the growth and differentiation of enteric NCCs during development. In this report, we further elucidate its role in neuroblastoma progression. Experimental Design: We studied the expression and copy number of EG-VEGF/Prok-1 receptors (PK-R1 and PK-R2) in 26 neuroblastoma tumors by real-time reverse transcription-PCR and immunohistochemical analysis. Implication of EG-VEGF/Prok-1 signaling in neuroblastoma progression was further shown in a neuroblastoma cell line (SK-N-SH). Results: We found that all neuroblastoma samples from stages II to IV expressed both PK-R1 and PK-R2. Kruskall-Wallis signed rank tests revealed that the expression level of PK-R1 transcript is associated with the stages and metastasis of the neuroblastoma (P < 0.05), and PK-R2 is persistently higher in advanced-stage neuroblastoma samples. About 38% of the neuroblastoma tumors (10:26) possessed MYCN amplification, whereas no PK-R1 and PK-R2 amplifications were detected, suggesting that the overexpression of the receptors was not due to gene amplification. Subsequent functional studies showed that EG-VEGF/Prok-1 activates the Akt pathway to induce the proliferation of neuroblastoma cells. Targeted down-regulation studies revealed that EG-VEGF/Prok-1 - mediated proliferation requires the presence of these two receptors, and that PK-R2 is essential for inhibiting apoptosis. In vitro migration and invasion assays also indicated that EG-VEGF/Prok-1 significantly enhances the cell migration/invasion of SK-N-SH. Conclusions: Our study has shown for the first time that aberrant EG-VEGF/Prok-1 signaling favors neuroblastoma progression and could be a potential target for future neuroblastoma treatment. © 2007 American Association for Cancer Research.
Persistent Identifierhttp://hdl.handle.net/10722/92286
ISSN
2015 Impact Factor: 8.738
2015 SCImago Journal Rankings: 5.314
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorNgan, ESWen_HK
dc.contributor.authorSit, FYLen_HK
dc.contributor.authorLee, Ken_HK
dc.contributor.authorMiao, Xen_HK
dc.contributor.authorYuan, Zen_HK
dc.contributor.authorWang, Wen_HK
dc.contributor.authorNicholls, JMen_HK
dc.contributor.authorWong, KKYen_HK
dc.contributor.authorGarciaBarcelo, Men_HK
dc.contributor.authorLui, VCHen_HK
dc.contributor.authorTam, PKHen_HK
dc.date.accessioned2010-09-17T10:41:34Z-
dc.date.available2010-09-17T10:41:34Z-
dc.date.issued2007en_HK
dc.identifier.citationClinical Cancer Research, 2007, v. 13 n. 3, p. 868-875en_HK
dc.identifier.issn1078-0432en_HK
dc.identifier.urihttp://hdl.handle.net/10722/92286-
dc.description.abstractPurpose: Neuroblastoma is a common pediatric tumor that is derived from improperly differentiated neural crest cells (NCC). We recently revealed that endocrine gland - derived vascular endothelial growth factor/prokineticin-1 (EG-VEGF/Prok-1) is a key factor mediating the growth and differentiation of enteric NCCs during development. In this report, we further elucidate its role in neuroblastoma progression. Experimental Design: We studied the expression and copy number of EG-VEGF/Prok-1 receptors (PK-R1 and PK-R2) in 26 neuroblastoma tumors by real-time reverse transcription-PCR and immunohistochemical analysis. Implication of EG-VEGF/Prok-1 signaling in neuroblastoma progression was further shown in a neuroblastoma cell line (SK-N-SH). Results: We found that all neuroblastoma samples from stages II to IV expressed both PK-R1 and PK-R2. Kruskall-Wallis signed rank tests revealed that the expression level of PK-R1 transcript is associated with the stages and metastasis of the neuroblastoma (P < 0.05), and PK-R2 is persistently higher in advanced-stage neuroblastoma samples. About 38% of the neuroblastoma tumors (10:26) possessed MYCN amplification, whereas no PK-R1 and PK-R2 amplifications were detected, suggesting that the overexpression of the receptors was not due to gene amplification. Subsequent functional studies showed that EG-VEGF/Prok-1 activates the Akt pathway to induce the proliferation of neuroblastoma cells. Targeted down-regulation studies revealed that EG-VEGF/Prok-1 - mediated proliferation requires the presence of these two receptors, and that PK-R2 is essential for inhibiting apoptosis. In vitro migration and invasion assays also indicated that EG-VEGF/Prok-1 significantly enhances the cell migration/invasion of SK-N-SH. Conclusions: Our study has shown for the first time that aberrant EG-VEGF/Prok-1 signaling favors neuroblastoma progression and could be a potential target for future neuroblastoma treatment. © 2007 American Association for Cancer Research.en_HK
dc.languageengen_HK
dc.publisherAmerican Association for Cancer Researchen_HK
dc.relation.ispartofClinical Cancer Researchen_HK
dc.subject.meshCell Movementen_HK
dc.subject.meshCell Proliferationen_HK
dc.subject.meshChilden_HK
dc.subject.meshChild, Preschoolen_HK
dc.subject.meshDisease Progressionen_HK
dc.subject.meshEndocrine Glands - metabolismen_HK
dc.subject.meshFemaleen_HK
dc.subject.meshGene Expression Regulation, Neoplasticen_HK
dc.subject.meshHumansen_HK
dc.subject.meshInfanten_HK
dc.subject.meshMaleen_HK
dc.subject.meshNeoplasm Invasivenessen_HK
dc.subject.meshNeuroblastoma - metabolism - pathologyen_HK
dc.subject.meshReverse Transcriptase Polymerase Chain Reactionen_HK
dc.subject.meshSignal Transductionen_HK
dc.subject.meshVascular Endothelial Growth Factor, Endocrine-Gland-Derived - metabolismen_HK
dc.titleImplications of endocrine gland - Derived vascular endothelial growth factor/prokineticin-1 signaling in human neuroblastoma progressionen_HK
dc.typeArticleen_HK
dc.identifier.emailNgan, ESW:engan@hkucc.hku.hken_HK
dc.identifier.emailNicholls, JM:nicholls@pathology.hku.hken_HK
dc.identifier.emailWong, KKY:kkywong@hkucc.hku.hken_HK
dc.identifier.emailGarciaBarcelo, M:mmgarcia@hkucc.hku.hken_HK
dc.identifier.emailLui, VCH:vchlui@hkucc.hku.hken_HK
dc.identifier.emailTam, PKH:paultam@hkucc.hku.hken_HK
dc.identifier.authorityNgan, ESW=rp00422en_HK
dc.identifier.authorityNicholls, JM=rp00364en_HK
dc.identifier.authorityWong, KKY=rp01392en_HK
dc.identifier.authorityGarciaBarcelo, M=rp00445en_HK
dc.identifier.authorityLui, VCH=rp00363en_HK
dc.identifier.authorityTam, PKH=rp00060en_HK
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1158/1078-0432.CCR-06-2176en_HK
dc.identifier.pmid17289879-
dc.identifier.scopuseid_2-s2.0-33847394476en_HK
dc.identifier.hkuros125997-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33847394476&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume13en_HK
dc.identifier.issue3en_HK
dc.identifier.spage868en_HK
dc.identifier.epage875en_HK
dc.identifier.eissn1557-3265-
dc.identifier.isiWOS:000244289400015-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridNgan, ESW=22234827500-
dc.identifier.scopusauthoridSit, FYL=16025577300-
dc.identifier.scopusauthoridLee, K=35074338500-
dc.identifier.scopusauthoridMiao, X=7102585391-
dc.identifier.scopusauthoridYuan, Z=10641253300-
dc.identifier.scopusauthoridWang, W=7501755015-
dc.identifier.scopusauthoridNicholls, JM=7201463077-
dc.identifier.scopusauthoridWong, KKY=24438686400-
dc.identifier.scopusauthoridGarciaBarcelo, M=6701767303-
dc.identifier.scopusauthoridLui, VCH=7004231344-
dc.identifier.scopusauthoridTam, PKH=7202539421-

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