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Article: Epigenetic identification of ADAMTS18 as a novel 16q23.1 tumor suppressor frequently silenced in esophageal, nasopharyngeal and multiple other carcinomas
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TitleEpigenetic identification of ADAMTS18 as a novel 16q23.1 tumor suppressor frequently silenced in esophageal, nasopharyngeal and multiple other carcinomas
 
AuthorsJin, H6
Wang, X6
Ying, J6
Wong, AHY6
Li, H6
Lee, KY6
Srivastava, G2
Chan, ATC6
Yeo, W6
Ma, BBY6
Putti, TC1
Lung, ML5
Shen, ZY3
Xu, LY3
Langford, C4
Tao, Q6 6
 
KeywordsADAMTS18
Carcinoma
Methylation
Promoter
Tumor suppressor gene
 
Issue Date2007
 
PublisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/onc
 
CitationOncogene, 2007, v. 26 n. 53, p. 7490-7498 [How to Cite?]
DOI: http://dx.doi.org/10.1038/sj.onc.1210559
 
AbstractTumor suppressor genes (TSGs) often locate at chromosomal regions with frequent deletions in tumors. Loss of 16q23 occurs frequently in multiple tumors, indicating the presence of critical TSGs at this locus, such as the well-studied WWOX. Herein, we found that ADAMTS18, located next to WWOX, was significantly downregulated in multiple carcinoma cell lines. No deletion of ADAMTS18 was detected with multiplex differential DNA-PCR or high-resolution 1-Mb array-based comparative genomic hybridization (CGH) analysis. Instead, methylation of the ADAMTS18 promoter CpG Island was frequently detected with methylation-specific PCR and bisulfite genome sequencing in multiple carcinoma cell lines and primary carcinomas, but not in any nontumor cell line and normal epithelial tissue. Both pharmacological and genetic demethylation dramatically induced the ADAMTS18 expression, indicating that CpG methylation directly contributes to the tumor-specific silencing of ADAMTS18. Ectopic ADAMTS18 expression led to significant inhibition of both anchorage-dependent and -independent growth of carcinoma cells lacking the expression. Thus, through functional epigenetics, we identified ADAMTS18 as a novel functional tumor suppressor, being frequently inactivated epigenetically in multiple carcinomas. © 2007 Nature Publishing Group All rights reserved.
 
ISSN0950-9232
2012 Impact Factor: 7.357
2012 SCImago Journal Rankings: 3.558
 
DOIhttp://dx.doi.org/10.1038/sj.onc.1210559
 
ISI Accession Number IDWOS:000251282000010
 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorJin, H
 
dc.contributor.authorWang, X
 
dc.contributor.authorYing, J
 
dc.contributor.authorWong, AHY
 
dc.contributor.authorLi, H
 
dc.contributor.authorLee, KY
 
dc.contributor.authorSrivastava, G
 
dc.contributor.authorChan, ATC
 
dc.contributor.authorYeo, W
 
dc.contributor.authorMa, BBY
 
dc.contributor.authorPutti, TC
 
dc.contributor.authorLung, ML
 
dc.contributor.authorShen, ZY
 
dc.contributor.authorXu, LY
 
dc.contributor.authorLangford, C
 
dc.contributor.authorTao, Q
 
dc.date.accessioned2012-05-29T06:13:31Z
 
dc.date.available2012-05-29T06:13:31Z
 
dc.date.issued2007
 
dc.description.abstractTumor suppressor genes (TSGs) often locate at chromosomal regions with frequent deletions in tumors. Loss of 16q23 occurs frequently in multiple tumors, indicating the presence of critical TSGs at this locus, such as the well-studied WWOX. Herein, we found that ADAMTS18, located next to WWOX, was significantly downregulated in multiple carcinoma cell lines. No deletion of ADAMTS18 was detected with multiplex differential DNA-PCR or high-resolution 1-Mb array-based comparative genomic hybridization (CGH) analysis. Instead, methylation of the ADAMTS18 promoter CpG Island was frequently detected with methylation-specific PCR and bisulfite genome sequencing in multiple carcinoma cell lines and primary carcinomas, but not in any nontumor cell line and normal epithelial tissue. Both pharmacological and genetic demethylation dramatically induced the ADAMTS18 expression, indicating that CpG methylation directly contributes to the tumor-specific silencing of ADAMTS18. Ectopic ADAMTS18 expression led to significant inhibition of both anchorage-dependent and -independent growth of carcinoma cells lacking the expression. Thus, through functional epigenetics, we identified ADAMTS18 as a novel functional tumor suppressor, being frequently inactivated epigenetically in multiple carcinomas. © 2007 Nature Publishing Group All rights reserved.
 
dc.description.natureLink_to_subscribed_fulltext
 
dc.identifier.citationOncogene, 2007, v. 26 n. 53, p. 7490-7498 [How to Cite?]
DOI: http://dx.doi.org/10.1038/sj.onc.1210559
 
dc.identifier.citeulike1373647
 
dc.identifier.doihttp://dx.doi.org/10.1038/sj.onc.1210559
 
dc.identifier.epage7498
 
dc.identifier.hkuros132779
 
dc.identifier.isiWOS:000251282000010
 
dc.identifier.issn0950-9232
2012 Impact Factor: 7.357
2012 SCImago Journal Rankings: 3.558
 
dc.identifier.issue53
 
dc.identifier.pmid17546048
 
dc.identifier.scopuseid_2-s2.0-34648817483
 
dc.identifier.spage7490
 
dc.identifier.urihttp://hdl.handle.net/10722/148525
 
dc.identifier.volume26
 
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.subject.meshAdam Proteins - Genetics
 
dc.subject.meshCell Growth Processes - Genetics
 
dc.subject.meshCell Line, Tumor
 
dc.subject.meshChromosomes, Human, Pair 16
 
dc.subject.meshDna Methylation
 
dc.subject.meshDown-Regulation
 
dc.subject.meshEsophageal Neoplasms - Genetics
 
dc.subject.meshFemale
 
dc.subject.meshGene Deletion
 
dc.subject.meshGene Expression Regulation, Neoplastic
 
dc.subject.meshGene Silencing
 
dc.subject.meshGenes, Tumor Suppressor
 
dc.subject.meshHela Cells
 
dc.subject.meshHumans
 
dc.subject.meshMale
 
dc.subject.meshNasopharyngeal Neoplasms - Genetics
 
dc.subject.meshNucleic Acid Hybridization
 
dc.subject.meshReverse Transcriptase Polymerase Chain Reaction
 
dc.subjectADAMTS18
 
dc.subjectCarcinoma
 
dc.subjectMethylation
 
dc.subjectPromoter
 
dc.subjectTumor suppressor gene
 
dc.titleEpigenetic identification of ADAMTS18 as a novel 16q23.1 tumor suppressor frequently silenced in esophageal, nasopharyngeal and multiple other carcinomas
 
dc.typeArticle
 
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Author Affiliations
  1. Yong Loo Lin School of Medicine
  2. The University of Hong Kong
  3. Shantou University, Medical College (SUMC)
  4. Wellcome Trust Sanger Institute
  5. Hong Kong University of Science and Technology
  6. Chinese University of Hong Kong