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Article: Monochromosome transfer and microarray analysis identify a critical tumor-suppressive region mapping to chromosome 13q14 and THSD1 in esophageal carcinoma
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TitleMonochromosome transfer and microarray analysis identify a critical tumor-suppressive region mapping to chromosome 13q14 and THSD1 in esophageal carcinoma
 
AuthorsKo, JMY4
Pui, LC4
Wing, LY4
Ho, KC4
King, CC4
Zhuo, YY4
Fung, MK4
Miller, LD2
Liu, ET2
Li, CY4
Lo, PHY4
Stanbridge, EJ5
Tang, JCO1 3
Srivastava, G1
Sai, WT1
Law, S1
Lung, ML4
 
Issue Date2008
 
PublisherAmerican Association for Cancer Research. The Journal's web site is located at http://mcr.aacrjournals.org/
 
CitationMolecular Cancer Research, 2008, v. 6 n. 4, p. 592-603 [How to Cite?]
DOI: http://dx.doi.org/10.1158/1541-7786.MCR-07-0154
 
AbstractLoss of chromosome 13q regions in esophageal squamous cell carcinoma (ESCC) is a frequent event. Monochromosome transfer approaches provide direct functional evidence for tumor suppression by chromosome 13 in SLMT-1, an ESCC cell line, and identify critical regions at 13q12.3, 13q14.11, and 13q14.3. Differential gene expression profiles of three tumor-suppressing microcell hybrids (MCH) and their tumorigenic parental SLMT-1 cell line were revealed by competitive hybridization using 19k cDNA oligonucleotide microarrays. Nine candidate 13q14 tumor-suppressor genes (TSG), including RB1, showed down-regulation in SLMT-1, compared with NE1, an immortalized normal esophageal epithelial cell line; their average gene expression was restored in MCHs compared with SLMT-1. Reverse transcription-PCR validated gene expression levels in MCHs and a panel of ESCC cell lines. Results suggest that the tumor-suppressing effect is not attributed to RB1, but instead likely involves thrombospondin type I domain-containing 1 (THSD1), a novel candidate TSG mapping to 13q14. Quantitative reverse transcription-PCR detected down-regulation of THSD1 expression in 100% of ESCC and other cancer cell lines. Mechanisms for THSD1 silencing in ESCC involved loss of heterozygosity and promoter hypermethylation, as analyzed by methylation-specific PCR and clonal bisulfite sequencing. Transfection of wild-type THSD1 into SLMT-1 resulted in significant reduction of colony-forming ability, hence providing functional evidence for its growth-suppressive activity. These findings suggest that THSD1 is a good candidate TSG. Copyright © 2008 American Association for Cancer Research.
 
ISSN1541-7786
2013 Impact Factor: 4.502
2013 SCImago Journal Rankings: 2.764
 
DOIhttp://dx.doi.org/10.1158/1541-7786.MCR-07-0154
 
ISI Accession Number IDWOS:000254905600009
 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorKo, JMY
 
dc.contributor.authorPui, LC
 
dc.contributor.authorWing, LY
 
dc.contributor.authorHo, KC
 
dc.contributor.authorKing, CC
 
dc.contributor.authorZhuo, YY
 
dc.contributor.authorFung, MK
 
dc.contributor.authorMiller, LD
 
dc.contributor.authorLiu, ET
 
dc.contributor.authorLi, CY
 
dc.contributor.authorLo, PHY
 
dc.contributor.authorStanbridge, EJ
 
dc.contributor.authorTang, JCO
 
dc.contributor.authorSrivastava, G
 
dc.contributor.authorSai, WT
 
dc.contributor.authorLaw, S
 
dc.contributor.authorLung, ML
 
dc.date.accessioned2010-09-06T05:58:08Z
 
dc.date.available2010-09-06T05:58:08Z
 
dc.date.issued2008
 
dc.description.abstractLoss of chromosome 13q regions in esophageal squamous cell carcinoma (ESCC) is a frequent event. Monochromosome transfer approaches provide direct functional evidence for tumor suppression by chromosome 13 in SLMT-1, an ESCC cell line, and identify critical regions at 13q12.3, 13q14.11, and 13q14.3. Differential gene expression profiles of three tumor-suppressing microcell hybrids (MCH) and their tumorigenic parental SLMT-1 cell line were revealed by competitive hybridization using 19k cDNA oligonucleotide microarrays. Nine candidate 13q14 tumor-suppressor genes (TSG), including RB1, showed down-regulation in SLMT-1, compared with NE1, an immortalized normal esophageal epithelial cell line; their average gene expression was restored in MCHs compared with SLMT-1. Reverse transcription-PCR validated gene expression levels in MCHs and a panel of ESCC cell lines. Results suggest that the tumor-suppressing effect is not attributed to RB1, but instead likely involves thrombospondin type I domain-containing 1 (THSD1), a novel candidate TSG mapping to 13q14. Quantitative reverse transcription-PCR detected down-regulation of THSD1 expression in 100% of ESCC and other cancer cell lines. Mechanisms for THSD1 silencing in ESCC involved loss of heterozygosity and promoter hypermethylation, as analyzed by methylation-specific PCR and clonal bisulfite sequencing. Transfection of wild-type THSD1 into SLMT-1 resulted in significant reduction of colony-forming ability, hence providing functional evidence for its growth-suppressive activity. These findings suggest that THSD1 is a good candidate TSG. Copyright © 2008 American Association for Cancer Research.
 
dc.description.naturelink_to_OA_fulltext
 
dc.identifier.citationMolecular Cancer Research, 2008, v. 6 n. 4, p. 592-603 [How to Cite?]
DOI: http://dx.doi.org/10.1158/1541-7786.MCR-07-0154
 
dc.identifier.doihttp://dx.doi.org/10.1158/1541-7786.MCR-07-0154
 
dc.identifier.epage603
 
dc.identifier.hkuros141625
 
dc.identifier.isiWOS:000254905600009
 
dc.identifier.issn1541-7786
2013 Impact Factor: 4.502
2013 SCImago Journal Rankings: 2.764
 
dc.identifier.issue4
 
dc.identifier.openurl
 
dc.identifier.pmid18403638
 
dc.identifier.scopuseid_2-s2.0-42049120045
 
dc.identifier.spage592
 
dc.identifier.urihttp://hdl.handle.net/10722/67774
 
dc.identifier.volume6
 
dc.languageeng
 
dc.publisherAmerican Association for Cancer Research. The Journal's web site is located at http://mcr.aacrjournals.org/
 
dc.publisher.placeUnited States
 
dc.relation.ispartofMolecular Cancer Research
 
dc.relation.referencesReferences in Scopus
 
dc.subject.meshAlleles
 
dc.subject.meshCell Line, Transformed
 
dc.subject.meshCell Line, Tumor
 
dc.subject.meshChromosome Mapping
 
dc.subject.meshChromosome Segregation
 
dc.subject.meshChromosomes, Human, Pair 13 - genetics
 
dc.subject.meshDNA Methylation - drug effects
 
dc.subject.meshDeoxycytidine - pharmacology
 
dc.subject.meshEpithelial Cells - drug effects - pathology
 
dc.subject.meshEsophageal Neoplasms - genetics
 
dc.subject.meshGene Expression Profiling
 
dc.subject.meshGene Expression Regulation, Neoplastic - drug effects
 
dc.subject.meshGenes, Tumor Suppressor
 
dc.subject.meshGenome, Human - genetics
 
dc.subject.meshHumans
 
dc.subject.meshHydroxamic Acids - pharmacology
 
dc.subject.meshIn Situ Hybridization, Fluorescence
 
dc.subject.meshMicroarray Analysis
 
dc.subject.meshMicrosatellite Repeats - genetics
 
dc.subject.meshPromoter Regions, Genetic - genetics
 
dc.subject.meshReverse Transcriptase Polymerase Chain Reaction
 
dc.subject.meshThrombospondins - genetics - metabolism
 
dc.subject.meshTransfection
 
dc.subject.meshTumor Stem Cell Assay
 
dc.titleMonochromosome transfer and microarray analysis identify a critical tumor-suppressive region mapping to chromosome 13q14 and THSD1 in esophageal carcinoma
 
dc.typeArticle
 
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<description.abstract>Loss of chromosome 13q regions in esophageal squamous cell carcinoma (ESCC) is a frequent event. Monochromosome transfer approaches provide direct functional evidence for tumor suppression by chromosome 13 in SLMT-1, an ESCC cell line, and identify critical regions at 13q12.3, 13q14.11, and 13q14.3. Differential gene expression profiles of three tumor-suppressing microcell hybrids (MCH) and their tumorigenic parental SLMT-1 cell line were revealed by competitive hybridization using 19k cDNA oligonucleotide microarrays. Nine candidate 13q14 tumor-suppressor genes (TSG), including RB1, showed down-regulation in SLMT-1, compared with NE1, an immortalized normal esophageal epithelial cell line; their average gene expression was restored in MCHs compared with SLMT-1. Reverse transcription-PCR validated gene expression levels in MCHs and a panel of ESCC cell lines. Results suggest that the tumor-suppressing effect is not attributed to RB1, but instead likely involves thrombospondin type I domain-containing 1 (THSD1), a novel candidate TSG mapping to 13q14. Quantitative reverse transcription-PCR detected down-regulation of THSD1 expression in 100% of ESCC and other cancer cell lines. Mechanisms for THSD1 silencing in ESCC involved loss of heterozygosity and promoter hypermethylation, as analyzed by methylation-specific PCR and clonal bisulfite sequencing. Transfection of wild-type THSD1 into SLMT-1 resulted in significant reduction of colony-forming ability, hence providing functional evidence for its growth-suppressive activity. These findings suggest that THSD1 is a good candidate TSG. Copyright &#169; 2008 American Association for Cancer Research.</description.abstract>
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Author Affiliations
  1. The University of Hong Kong
  2. Genome Institute of Singapore
  3. Hong Kong Polytechnic University
  4. Hong Kong University of Science and Technology
  5. UC Irvine