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Article: RASSF1A is a target tumor suppressor from 3p21.3 in nasopharyngeal carcinoma

TitleRASSF1A is a target tumor suppressor from 3p21.3 in nasopharyngeal carcinoma
Authors
Issue Date2004
PublisherJohn Wiley & Sons, Inc.. The Journal's web site is located at http://www3.interscience.wiley.com/journal/29331/home
Citation
International Journal Of Cancer, 2004, v. 109 n. 6, p. 839-847 How to Cite?
AbstractDeletion on the short arm of chromosome 3 is one of the most important genetic abnormalities in the tumorigenesis of nasopharyngeal carcinoma (NPC). Both physical mapping and functional studies have targeted an NPC-related tumor suppressor gene(s) to chromosome 3p21.3. We have reported recently that RASSF1A gene, located on a 120-kb minimal deletion region on 3p21.3, was frequently inactivated by promoter hypermethylation in NPC. We further confirmed that RASSF1A is the critical target tumor suppressor from 3p21.3, with the evidence that loss of expression and aberrant methylation of the other 8 candidate genes/transcripts (HYAL2, FUS1, RASSF1C, BLU, NPRL2, 101F6, PL6 and CACNA2D2) in this 120-kb region were rare in NPC samples. The contribution of RASSF1A in NPC tumorigenesis was investigated by restoring its expression in a RASSF1A deficient cell line, C666-1. Transient transfection of wild-type RASSF1A resulted in marked growth inhibition in NPC cells. Isolated stable clones expressing wild-type RASSF1A demonstrated retarded cell proliferation in vitro. Soft-agar assay also showed decreased number and sizes of colony formed in these clones. In vivo nude mice assay demonstrated the dramatic reduction of tumorigenic potential in the RASSF1A-transfected clones. Our results provide strong evidence to support RASSF1A as a target tumor suppressor gene on 3p21.3 in NPC. © 2004 Wiley-Liss, Inc.
Persistent Identifierhttp://hdl.handle.net/10722/148427
ISSN
2015 Impact Factor: 5.531
2015 SCImago Journal Rankings: 2.657
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorChow, LSNen_US
dc.contributor.authorLo, KWen_US
dc.contributor.authorKwong, Jen_US
dc.contributor.authorTo, KFen_US
dc.contributor.authorTsang, KSen_US
dc.contributor.authorLam, CWen_US
dc.contributor.authorDammann, Ren_US
dc.contributor.authorHuang, DPen_US
dc.date.accessioned2012-05-29T06:12:55Z-
dc.date.available2012-05-29T06:12:55Z-
dc.date.issued2004en_US
dc.identifier.citationInternational Journal Of Cancer, 2004, v. 109 n. 6, p. 839-847en_US
dc.identifier.issn0020-7136en_US
dc.identifier.urihttp://hdl.handle.net/10722/148427-
dc.description.abstractDeletion on the short arm of chromosome 3 is one of the most important genetic abnormalities in the tumorigenesis of nasopharyngeal carcinoma (NPC). Both physical mapping and functional studies have targeted an NPC-related tumor suppressor gene(s) to chromosome 3p21.3. We have reported recently that RASSF1A gene, located on a 120-kb minimal deletion region on 3p21.3, was frequently inactivated by promoter hypermethylation in NPC. We further confirmed that RASSF1A is the critical target tumor suppressor from 3p21.3, with the evidence that loss of expression and aberrant methylation of the other 8 candidate genes/transcripts (HYAL2, FUS1, RASSF1C, BLU, NPRL2, 101F6, PL6 and CACNA2D2) in this 120-kb region were rare in NPC samples. The contribution of RASSF1A in NPC tumorigenesis was investigated by restoring its expression in a RASSF1A deficient cell line, C666-1. Transient transfection of wild-type RASSF1A resulted in marked growth inhibition in NPC cells. Isolated stable clones expressing wild-type RASSF1A demonstrated retarded cell proliferation in vitro. Soft-agar assay also showed decreased number and sizes of colony formed in these clones. In vivo nude mice assay demonstrated the dramatic reduction of tumorigenic potential in the RASSF1A-transfected clones. Our results provide strong evidence to support RASSF1A as a target tumor suppressor gene on 3p21.3 in NPC. © 2004 Wiley-Liss, Inc.en_US
dc.languageengen_US
dc.publisherJohn Wiley & Sons, Inc.. The Journal's web site is located at http://www3.interscience.wiley.com/journal/29331/homeen_US
dc.relation.ispartofInternational Journal of Canceren_US
dc.subject.meshAnimalsen_US
dc.subject.meshAzacitidine - Pharmacologyen_US
dc.subject.meshCell Cycleen_US
dc.subject.meshCell Division - Geneticsen_US
dc.subject.meshChromosomes, Human, Pair 3 - Geneticsen_US
dc.subject.meshColony-Forming Units Assayen_US
dc.subject.meshDna Methylationen_US
dc.subject.meshFemaleen_US
dc.subject.meshGene Expression Regulation, Neoplasticen_US
dc.subject.meshGenes, Tumor Suppressoren_US
dc.subject.meshHumansen_US
dc.subject.meshMiceen_US
dc.subject.meshMice, Inbred Balb Cen_US
dc.subject.meshMice, Nudeen_US
dc.subject.meshNasopharyngeal Neoplasms - Genetics - Metabolism - Pathologyen_US
dc.subject.meshNasopharynx - Metabolism - Pathologyen_US
dc.subject.meshReverse Transcriptase Polymerase Chain Reactionen_US
dc.subject.meshTransduction, Geneticen_US
dc.subject.meshTumor Cells, Cultureden_US
dc.subject.meshTumor Markers, Biological - Genetics - Metabolismen_US
dc.subject.meshTumor Suppressor Proteins - Genetics - Metabolismen_US
dc.subject.meshXenograft Model Antitumor Assaysen_US
dc.titleRASSF1A is a target tumor suppressor from 3p21.3 in nasopharyngeal carcinomaen_US
dc.typeArticleen_US
dc.identifier.emailLam, CW:ching-wanlam@pathology.hku.hken_US
dc.identifier.authorityLam, CW=rp00260en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1002/ijc.20079en_US
dc.identifier.pmid15027117-
dc.identifier.scopuseid_2-s2.0-2442482316en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-2442482316&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume109en_US
dc.identifier.issue6en_US
dc.identifier.spage839en_US
dc.identifier.epage847en_US
dc.identifier.isiWOS:000220779200006-
dc.publisher.placeUnited Statesen_US

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