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Article: Involvement of visinin-like protein-1 (VSNL-1) in regulating proliferative and invasive properties of neuroblastoma

TitleInvolvement of visinin-like protein-1 (VSNL-1) in regulating proliferative and invasive properties of neuroblastoma
Authors
Issue Date2007
PublisherOxford University Press. The Journal's web site is located at http://carcin.oxfordjournals.org/
Citation
Carcinogenesis, 2007, v. 28 n. 10, p. 2122-2130 How to Cite?
AbstractTumor Growth And Metastasis Require That Tumor Cells Must Have Either The Potential To Shift Genetically Or Epigenetically Between Proliferative And Invasive Phenotypes Or Both Phenotypes Simultaneously. In The Present Study, We Demonstrated That Neuroblastoma Growth And Invasion Were Distinct Processes That Were Carried Out By Proliferative And Invasive Phenotypes Of Tumor Cells, Respectively. Two Subpopulations From Human Neuroblastoma Cell Line Were Isolated: Highly Invasive (Hi) Cells And Low-Invasive (Li) Cells. Hi And Li Cells Had Different Proliferative Rate And Metastatic Ability In Vitro And In Vivo. In Addition, They Had Distinct Activated Signal Pathways And Sensitivities To Chemotherapy Drugs. Affymetrix Microarray And Quantitative Reverse Transcriptase-Polymerase Chain Reaction Revealed That Visinin-Like Protein-1 (Vsnl-1) Mrna In Hi Cells Was Significantly Higher Than That In Li Cells. We Also Observed That Vsnl-1 Was Over-Expressed In Tumor Specimens From Patients With Distant Organ Metastases Compared With Those Without Metastases. Furthermore, The Invasive And Proliferative Phenotypes Of Neuroblastoma Cells Could Be Exchanged By Regulation Of Vsnl-1 Expression In Vitro And In Vivo. Up-Regulation Of Vsnl-1 Potentiated The Anoikis-Resistant Ability Of Neuroblastoma Cell. The Expression Of Anoikis Inhibitor Trkb, Intracellular Adhesion Molecule 1, Major Histocompatibility Complex Class I, Cd44 And Cd44v6 Was Associated With Vsnl-1 Level. These Results Suggested That Distinct Roles Of Proliferative And Invasive Phenotypes Contributed To Neuroblastoma Progression And Strongly Demonstrated That Vsnl-1 Played A Very Important Role In Neuroblastoma Metastasis. © The Author 2007. Published By Oxford University Press. All Rights Reserved.
Persistent Identifierhttp://hdl.handle.net/10722/83231
ISSN
2015 Impact Factor: 4.874
2015 SCImago Journal Rankings: 2.439
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorXie, Yen_HK
dc.contributor.authorChan, HMen_HK
dc.contributor.authorFan, Jen_HK
dc.contributor.authorChen, Yen_HK
dc.contributor.authorYoung, Jen_HK
dc.contributor.authorLi, Wen_HK
dc.contributor.authorMiao, Xen_HK
dc.contributor.authorYuan, Zen_HK
dc.contributor.authorWang, HMen_HK
dc.contributor.authorTam, PKHen_HK
dc.contributor.authorRen, Yen_HK
dc.date.accessioned2010-09-06T08:38:34Z-
dc.date.available2010-09-06T08:38:34Z-
dc.date.issued2007en_HK
dc.identifier.citationCarcinogenesis, 2007, v. 28 n. 10, p. 2122-2130en_HK
dc.identifier.issn0143-3334en_HK
dc.identifier.urihttp://hdl.handle.net/10722/83231-
dc.description.abstractTumor Growth And Metastasis Require That Tumor Cells Must Have Either The Potential To Shift Genetically Or Epigenetically Between Proliferative And Invasive Phenotypes Or Both Phenotypes Simultaneously. In The Present Study, We Demonstrated That Neuroblastoma Growth And Invasion Were Distinct Processes That Were Carried Out By Proliferative And Invasive Phenotypes Of Tumor Cells, Respectively. Two Subpopulations From Human Neuroblastoma Cell Line Were Isolated: Highly Invasive (Hi) Cells And Low-Invasive (Li) Cells. Hi And Li Cells Had Different Proliferative Rate And Metastatic Ability In Vitro And In Vivo. In Addition, They Had Distinct Activated Signal Pathways And Sensitivities To Chemotherapy Drugs. Affymetrix Microarray And Quantitative Reverse Transcriptase-Polymerase Chain Reaction Revealed That Visinin-Like Protein-1 (Vsnl-1) Mrna In Hi Cells Was Significantly Higher Than That In Li Cells. We Also Observed That Vsnl-1 Was Over-Expressed In Tumor Specimens From Patients With Distant Organ Metastases Compared With Those Without Metastases. Furthermore, The Invasive And Proliferative Phenotypes Of Neuroblastoma Cells Could Be Exchanged By Regulation Of Vsnl-1 Expression In Vitro And In Vivo. Up-Regulation Of Vsnl-1 Potentiated The Anoikis-Resistant Ability Of Neuroblastoma Cell. The Expression Of Anoikis Inhibitor Trkb, Intracellular Adhesion Molecule 1, Major Histocompatibility Complex Class I, Cd44 And Cd44v6 Was Associated With Vsnl-1 Level. These Results Suggested That Distinct Roles Of Proliferative And Invasive Phenotypes Contributed To Neuroblastoma Progression And Strongly Demonstrated That Vsnl-1 Played A Very Important Role In Neuroblastoma Metastasis. © The Author 2007. Published By Oxford University Press. All Rights Reserved.en_US
dc.languageengen_HK
dc.publisherOxford University Press. The Journal's web site is located at http://carcin.oxfordjournals.org/en_HK
dc.relation.ispartofCarcinogenesisen_HK
dc.rightsCarcinogenesis. Copyright © Oxford University Press.en_HK
dc.titleInvolvement of visinin-like protein-1 (VSNL-1) in regulating proliferative and invasive properties of neuroblastomaen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0143-3334&volume=28&issue=10&spage=2122&epage=2130&date=2007&atitle=Involvement+of+visinin-like+protein-1+(VSNL-1)+in+regulating+proliferative+and+invasive+properties+of+neuroblastomaen_HK
dc.identifier.emailChen, Y: swakchenyj@hotmail.comen_HK
dc.identifier.emailMiao, X: miaoxp@hkucc.hku.hken_HK
dc.identifier.emailYuan, Z: yuanzw@hotmail.comen_HK
dc.identifier.emailTam, PKH: paultam@hkucc.hku.hken_HK
dc.identifier.emailRen, Y: yren@hkucc.hku.hken_HK
dc.identifier.authorityTam, PKH=rp00060en_HK
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1093/carcin/bgm147en_US
dc.identifier.pmid17615261-
dc.identifier.scopuseid_2-s2.0-35148837124en_US
dc.identifier.hkuros139459en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-35148837124&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume28en_US
dc.identifier.issue10en_US
dc.identifier.spage2122en_US
dc.identifier.epage2130en_US
dc.identifier.isiWOS:000250676400009-

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