Article: Anti-angiogenic and tumor-suppressive roles of candidate tumor-suppressor gene, Fibulin-2, in nasopharyngeal carcinoma

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TitleAnti-angiogenic and tumor-suppressive roles of candidate tumor-suppressor gene, Fibulin-2, in nasopharyngeal carcinoma
AuthorsLaw, EWL1
Cheung, AKL1
Kashuba, VI6
Pavlova, TV6
Zabarovsky, ER3 6
Lung, HL1
Cheng, Y1
Chua, D1 5
LaiWan Kwong, D1
Tsao, SW1
Sasaki, T4
Stanbridge, EJ2
Lung, ML1
Keywordsanti-angiogenic
fibulin-2
methylation
nasopharyngeal carcinoma
tumor suppressor
VEGF
Issue Date2012
PublisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/onc
CitationOncogene, 2012, v. 31 n. 6, p. 728-738 [How to Cite?]
DOI: http://dx.doi.org/10.1038/onc.2011.272
AbstractFibulin-2 (FBLN2) has been identified as a candidate tumor-suppressor gene in nasopharyngeal carcinoma (NPC). Originally identified through a chromosome 3 NotI genomic microarray screen, it shows frequent deletion or methylation in NPC. FBLN2 is located on chromosome 3p25.1 and is associated with tumor development through its important interactions with the extracellular matrix (ECM) proteins. FBLN2 encodes two isoforms. The short isoform (FBLN2S) is expressed abundantly in normal tissues, but is dramatically downregulated in NPC, while the long isoform (FBLN2L) is either not detectable or is expressed only at low levels in both normal and tumor tissues. Reintroduction of this FBLN2S inhibited cell proliferation, migration, invasion and angiogenesis in vitro. Furthermore, in vivo studies in nude mice show its expression is associated with tumor and angiogenesis suppression. FBLN2-associated angiogenesis occurs via concomitant downregulation of vascular endothelial growth factor and matrix metalloproteinase 2. This study provides compelling evidence that FBLN2S has an important tumor-suppressive and anti-angiogenic role in NPC. © 2012 Macmillan Publishers Limited All rights reserved.
ISSN0950-9232
2011 Impact Factor: 6.373
2011 SCImago Journal Rankings: 1.216
DOIhttp://dx.doi.org/10.1038/onc.2011.272
ISI Accession Number IDWOS:000300222100006
Funding AgencyGrant Number
University Grants CouncilAoE/M-06/08
Swedish Cancer Society
Swedish Research Council
Swedish Institute
Karolinska Institute
Funding Information:

This work was supported by University Grants Council Area of Excellence grant AoE/M-06/08 to MLL and the Swedish Cancer Society, the Swedish Research Council, the Swedish Institute, and Karolinska Institute to ERZ.

ReferencesReferences in Scopus
GrantsCentre for Nasopharyngeal Carcinoma Research
DC Field
Value
dc.contributor.authorLaw, EWL
dc.contributor.authorCheung, AKL
dc.contributor.authorKashuba, VI
dc.contributor.authorPavlova, TV
dc.contributor.authorZabarovsky, ER
dc.contributor.authorLung, HL
dc.contributor.authorCheng, Y
dc.contributor.authorChua, D
dc.contributor.authorLaiWan Kwong, D
dc.contributor.authorTsao, SW
dc.contributor.authorSasaki, T
dc.contributor.authorStanbridge, EJ
dc.contributor.authorLung, ML
dc.date.accessioned2011-06-17T09:19:16Z
dc.date.available2011-06-17T09:19:16Z
dc.date.issued2012
dc.description.abstractFibulin-2 (FBLN2) has been identified as a candidate tumor-suppressor gene in nasopharyngeal carcinoma (NPC). Originally identified through a chromosome 3 NotI genomic microarray screen, it shows frequent deletion or methylation in NPC. FBLN2 is located on chromosome 3p25.1 and is associated with tumor development through its important interactions with the extracellular matrix (ECM) proteins. FBLN2 encodes two isoforms. The short isoform (FBLN2S) is expressed abundantly in normal tissues, but is dramatically downregulated in NPC, while the long isoform (FBLN2L) is either not detectable or is expressed only at low levels in both normal and tumor tissues. Reintroduction of this FBLN2S inhibited cell proliferation, migration, invasion and angiogenesis in vitro. Furthermore, in vivo studies in nude mice show its expression is associated with tumor and angiogenesis suppression. FBLN2-associated angiogenesis occurs via concomitant downregulation of vascular endothelial growth factor and matrix metalloproteinase 2. This study provides compelling evidence that FBLN2S has an important tumor-suppressive and anti-angiogenic role in NPC. © 2012 Macmillan Publishers Limited All rights reserved.
dc.description.grantCentre for Nasopharyngeal Carcinoma Research
dc.description.grantcode101179
dc.description.natureLink_to_subscribed_fulltext
dc.identifier.citationOncogene, 2012, v. 31 n. 6, p. 728-738 [How to Cite?]
DOI: http://dx.doi.org/10.1038/onc.2011.272
dc.identifier.citeulike9543910
dc.identifier.doihttp://dx.doi.org/10.1038/onc.2011.272
dc.identifier.epage738
dc.identifier.hkuros185871
dc.identifier.isiWOS:000300222100006
Funding AgencyGrant Number
University Grants CouncilAoE/M-06/08
Swedish Cancer Society
Swedish Research Council
Swedish Institute
Karolinska Institute
Funding Information:

This work was supported by University Grants Council Area of Excellence grant AoE/M-06/08 to MLL and the Swedish Cancer Society, the Swedish Research Council, the Swedish Institute, and Karolinska Institute to ERZ.

dc.identifier.issn0950-9232
2011 Impact Factor: 6.373
2011 SCImago Journal Rankings: 1.216
dc.identifier.issue6
dc.identifier.openurl
dc.identifier.pmid21743496
dc.identifier.scopuseid_2-s2.0-84856949774
dc.identifier.spage728
dc.identifier.urihttp://hdl.handle.net/10722/134395
dc.identifier.volume31
dc.languageeng
dc.publisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/onc
dc.publisher.placeUnited Kingdom
dc.relation.ispartofOncogene
dc.relation.referencesReferences in Scopus
dc.subjectanti-angiogenic
dc.subjectfibulin-2
dc.subjectmethylation
dc.subjectnasopharyngeal carcinoma
dc.subjecttumor suppressor
dc.subjectVEGF
dc.titleAnti-angiogenic and tumor-suppressive roles of candidate tumor-suppressor gene, Fibulin-2, in nasopharyngeal carcinoma
dc.typeArticle
Author Affiliations
  1. The University of Hong Kong
  2. UC Irvine
  3. Engelhardt Institute of Molecular Biology, Russian Academy of Sciences
  4. null
  5. Hong Kong Sanatorium and Hospital
  6. Södersjukhuset