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Article: Identification of an invasion and tumor-suppressing gene, Endoglin (ENG), silenced by both epigenetic inactivation and allelic loss in esophageal squamous cell carcinoma

TitleIdentification of an invasion and tumor-suppressing gene, Endoglin (ENG), silenced by both epigenetic inactivation and allelic loss in esophageal squamous cell carcinoma
Authors
KeywordsEndoglin
Esophageal squamous cell carcinoma
Invasion
Loss of heterozygosity
Methylation
Tumorigenesis
Issue Date2008
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, 2008, v. 123 n. 12, p. 2816-2823 How to Cite?
AbstractEndoglin (ENG) has been identified as a candidate tumor-suppressor gene in esophageal squamous cell carcinoma (ESCC). Earlier microcell-mediated chromosome transfer (MMCT) studies of chromosome 9 in ESCC narrowed down a tumor-suppressive critical region to 9q33-34. ENG maps to 9q34-qter and encodes a transformation growth factor beta (TGFb) superfamily auxiliary receptor. This study aims to identify the potential role for ENG in ESCC development. Significant downregulation of ENG was detected at frequencies of 87.5% in 16 ESCC cell lines, 39.1% directly in 23 ESCC tumor specimens from Hong Kong, and 33.4% in 18 ESCC tumor specimens from the high-risk ESCC region of Henan, China. By methylation-specific PCR, methylated sequences were detected in an ESCC cell line panel and in clinical specimens. Following demethylation treatment in 9 ESCC cell lines, ENG expression was obviously restored. Loss of heterozygosity (LOH) in a 4.7 Mb region on 9q32-q34, where ENG maps, was observed directly in ESCC tumor tissues. Both epigenetic methylation and allelic loss appear to contribute to ENG downregulation in tumor cells. In vitro and in vivo functional studies such as colony formation, Matrigel culture, invasion and tumorigenicity assays were performed. Colony formation efficiency was significantly reduced by overexpression of ENG. In addition, significantly smaller colonies of ENG stable transfectants were formed in Matrigel culture. Significant suppression of invasion efficiency and tumorigenicity were also observed, when comparing the ENG stable transfectants with the vector-alone transfectants. This study provides evidence supporting ENG, as a cell invasion and tumor-suppressing gene in ESCC. © 2008 Wiley-Liss, Inc.
Persistent Identifierhttp://hdl.handle.net/10722/58185
ISSN
2015 Impact Factor: 5.531
2015 SCImago Journal Rankings: 2.657
ISI Accession Number ID
Funding AgencyGrant Number
Research Grants Council of the Hong Kong Special Administration Region, ChinaHKUST6467/05M
Ministerio de Educacion y Ciencia of SpainSAF2007-61827
Funding Information:

Grant sponsor: Research Grants Council of the Hong Kong Special Administration Region, China: Grant number: HKUST6467/05M. Grant sponsor: Ministerio de Educacion y Ciencia of Spain: Grant number: SAF2007-61827.

References

 

DC FieldValueLanguage
dc.contributor.authorWong, VCLen_HK
dc.contributor.authorPui, LCen_HK
dc.contributor.authorBernabeu, Cen_HK
dc.contributor.authorLaw, Sen_HK
dc.contributor.authorLi, DWen_HK
dc.contributor.authorLi, JNen_HK
dc.contributor.authorSai, WTen_HK
dc.contributor.authorSrivastava, Gen_HK
dc.contributor.authorLung, MLen_HK
dc.date.accessioned2010-05-31T03:25:25Z-
dc.date.available2010-05-31T03:25:25Z-
dc.date.issued2008en_HK
dc.identifier.citationInternational Journal Of Cancer, 2008, v. 123 n. 12, p. 2816-2823en_HK
dc.identifier.issn0020-7136en_HK
dc.identifier.urihttp://hdl.handle.net/10722/58185-
dc.description.abstractEndoglin (ENG) has been identified as a candidate tumor-suppressor gene in esophageal squamous cell carcinoma (ESCC). Earlier microcell-mediated chromosome transfer (MMCT) studies of chromosome 9 in ESCC narrowed down a tumor-suppressive critical region to 9q33-34. ENG maps to 9q34-qter and encodes a transformation growth factor beta (TGFb) superfamily auxiliary receptor. This study aims to identify the potential role for ENG in ESCC development. Significant downregulation of ENG was detected at frequencies of 87.5% in 16 ESCC cell lines, 39.1% directly in 23 ESCC tumor specimens from Hong Kong, and 33.4% in 18 ESCC tumor specimens from the high-risk ESCC region of Henan, China. By methylation-specific PCR, methylated sequences were detected in an ESCC cell line panel and in clinical specimens. Following demethylation treatment in 9 ESCC cell lines, ENG expression was obviously restored. Loss of heterozygosity (LOH) in a 4.7 Mb region on 9q32-q34, where ENG maps, was observed directly in ESCC tumor tissues. Both epigenetic methylation and allelic loss appear to contribute to ENG downregulation in tumor cells. In vitro and in vivo functional studies such as colony formation, Matrigel culture, invasion and tumorigenicity assays were performed. Colony formation efficiency was significantly reduced by overexpression of ENG. In addition, significantly smaller colonies of ENG stable transfectants were formed in Matrigel culture. Significant suppression of invasion efficiency and tumorigenicity were also observed, when comparing the ENG stable transfectants with the vector-alone transfectants. This study provides evidence supporting ENG, as a cell invasion and tumor-suppressing gene in ESCC. © 2008 Wiley-Liss, Inc.en_HK
dc.languageengen_HK
dc.publisherJohn Wiley & Sons, Inc.. The Journal's web site is located at http://www3.interscience.wiley.com/journal/29331/homeen_HK
dc.relation.ispartofInternational Journal of Canceren_HK
dc.rightsInternational Journal of Cancer. Copyright © John Wiley & Sons, Inc.en_HK
dc.subjectEndoglinen_HK
dc.subjectEsophageal squamous cell carcinomaen_HK
dc.subjectInvasionen_HK
dc.subjectLoss of heterozygosityen_HK
dc.subjectMethylationen_HK
dc.subjectTumorigenesisen_HK
dc.subject.meshAgeden_HK
dc.subject.meshAntigens, CD - analysis - geneticsen_HK
dc.subject.meshBlotting, Westernen_HK
dc.subject.meshCarcinoma, Squamous Cell - chemistry - genetics - immunology - secondaryen_HK
dc.subject.meshCell Line, Tumoren_HK
dc.subject.meshCell Proliferationen_HK
dc.subject.meshChinaen_HK
dc.subject.meshCollagenen_HK
dc.subject.meshDNA Methylationen_HK
dc.subject.meshDown-Regulationen_HK
dc.subject.meshDrug Combinationsen_HK
dc.subject.meshEsophageal Neoplasms - chemistry - genetics - pathologyen_HK
dc.subject.meshFemaleen_HK
dc.subject.meshGene Expression Profilingen_HK
dc.subject.meshGene Expression Regulation, Neoplasticen_HK
dc.subject.meshGene Silencingen_HK
dc.subject.meshHong Kongen_HK
dc.subject.meshHumansen_HK
dc.subject.meshLamininen_HK
dc.subject.meshLoss of Heterozygosityen_HK
dc.subject.meshLymphatic Metastasisen_HK
dc.subject.meshMaleen_HK
dc.subject.meshMicrosatellite Repeatsen_HK
dc.subject.meshMiddle Ageden_HK
dc.subject.meshNeoplasm Invasivenessen_HK
dc.subject.meshNeoplasm Stagingen_HK
dc.subject.meshPlasmidsen_HK
dc.subject.meshPromoter Regions, Geneticen_HK
dc.subject.meshProteoglycansen_HK
dc.subject.meshReceptors, Cell Surface - analysis - geneticsen_HK
dc.subject.meshReverse Transcriptase Polymerase Chain Reactionen_HK
dc.subject.meshSurvival Analysisen_HK
dc.subject.meshTransfectionen_HK
dc.subject.meshTumor Stem Cell Assayen_HK
dc.subject.meshTumor Suppressor Proteins - analysis - geneticsen_HK
dc.titleIdentification of an invasion and tumor-suppressing gene, Endoglin (ENG), silenced by both epigenetic inactivation and allelic loss in esophageal squamous cell carcinomaen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0020-7136&volume=123&issue=12&spage=2816&epage=2823&date=2008&atitle=Identification+of+an+invasion+and+tumor-suppressing+gene,+Endoglin+(ENG),+silenced+by+both+epigenetic+inactivation+and+allelic+loss+in+esophageal+squamous+cell+carcinomaen_HK
dc.identifier.emailLaw, S: slaw@hku.hken_HK
dc.identifier.emailSai, WT: gswtsao@hkucc.hku.hken_HK
dc.identifier.emailSrivastava, G: gopesh@pathology.hku.hken_HK
dc.identifier.emailLung, ML: mlilung@hku.hken_HK
dc.identifier.authorityLaw, S=rp00437en_HK
dc.identifier.authoritySai, WT=rp00399en_HK
dc.identifier.authoritySrivastava, G=rp00365en_HK
dc.identifier.authorityLung, ML=rp00300en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1002/ijc.23882en_HK
dc.identifier.pmid18798555en_HK
dc.identifier.scopuseid_2-s2.0-57349117010en_HK
dc.identifier.hkuros153328en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-57349117010&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume123en_HK
dc.identifier.issue12en_HK
dc.identifier.spage2816en_HK
dc.identifier.epage2823en_HK
dc.identifier.isiWOS:000261112900012-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridWong, VCL=23096631300en_HK
dc.identifier.scopusauthoridPui, LC=23095469900en_HK
dc.identifier.scopusauthoridBernabeu, C=7005583756en_HK
dc.identifier.scopusauthoridLaw, S=7202241293en_HK
dc.identifier.scopusauthoridLi, DW=27167922200en_HK
dc.identifier.scopusauthoridLi, JN=25825173700en_HK
dc.identifier.scopusauthoridSai, WT=7102813116en_HK
dc.identifier.scopusauthoridSrivastava, G=7202242238en_HK
dc.identifier.scopusauthoridLung, ML=7006411788en_HK

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