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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

TitleEpigenetic identification of ADAMTS18 as a novel 16q23.1 tumor suppressor frequently silenced in esophageal, nasopharyngeal and multiple other carcinomas
Authors
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
Citation
Oncogene, 2007, v. 26 n. 53, p. 7490-7498 How to Cite?
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.
Persistent Identifierhttp://hdl.handle.net/10722/148525
ISSN
2014 Impact Factor: 8.459
2014 SCImago Journal Rankings: 3.643
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorJin, Hen_HK
dc.contributor.authorWang, Xen_HK
dc.contributor.authorYing, Jen_HK
dc.contributor.authorWong, AHYen_HK
dc.contributor.authorLi, Hen_HK
dc.contributor.authorLee, KYen_HK
dc.contributor.authorSrivastava, Gen_HK
dc.contributor.authorChan, ATCen_HK
dc.contributor.authorYeo, Wen_HK
dc.contributor.authorMa, BBYen_HK
dc.contributor.authorPutti, TCen_HK
dc.contributor.authorLung, MLen_HK
dc.contributor.authorShen, ZYen_HK
dc.contributor.authorXu, LYen_HK
dc.contributor.authorLangford, Cen_HK
dc.contributor.authorTao, Qen_HK
dc.date.accessioned2012-05-29T06:13:31Z-
dc.date.available2012-05-29T06:13:31Z-
dc.date.issued2007en_HK
dc.identifier.citationOncogene, 2007, v. 26 n. 53, p. 7490-7498en_HK
dc.identifier.issn0950-9232en_HK
dc.identifier.urihttp://hdl.handle.net/10722/148525-
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.en_HK
dc.languageengen_US
dc.publisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/oncen_HK
dc.relation.ispartofOncogeneen_HK
dc.subjectADAMTS18en_HK
dc.subjectCarcinomaen_HK
dc.subjectMethylationen_HK
dc.subjectPromoteren_HK
dc.subjectTumor suppressor geneen_HK
dc.subject.meshAdam Proteins - Geneticsen_US
dc.subject.meshCell Growth Processes - Geneticsen_US
dc.subject.meshCell Line, Tumoren_US
dc.subject.meshChromosomes, Human, Pair 16en_US
dc.subject.meshDna Methylationen_US
dc.subject.meshDown-Regulationen_US
dc.subject.meshEsophageal Neoplasms - Geneticsen_US
dc.subject.meshFemaleen_US
dc.subject.meshGene Deletionen_US
dc.subject.meshGene Expression Regulation, Neoplasticen_US
dc.subject.meshGene Silencingen_US
dc.subject.meshGenes, Tumor Suppressoren_US
dc.subject.meshHela Cellsen_US
dc.subject.meshHumansen_US
dc.subject.meshMaleen_US
dc.subject.meshNasopharyngeal Neoplasms - Geneticsen_US
dc.subject.meshNucleic Acid Hybridizationen_US
dc.subject.meshReverse Transcriptase Polymerase Chain Reactionen_US
dc.titleEpigenetic identification of ADAMTS18 as a novel 16q23.1 tumor suppressor frequently silenced in esophageal, nasopharyngeal and multiple other carcinomasen_HK
dc.typeArticleen_HK
dc.identifier.emailSrivastava, G:gopesh@pathology.hku.hken_HK
dc.identifier.emailLung, ML:mlilung@hku.hken_HK
dc.identifier.authoritySrivastava, G=rp00365en_HK
dc.identifier.authorityLung, ML=rp00300en_HK
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1038/sj.onc.1210559en_HK
dc.identifier.pmid17546048en_HK
dc.identifier.scopuseid_2-s2.0-34648817483en_HK
dc.identifier.hkuros132779-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-34648817483&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume26en_HK
dc.identifier.issue53en_HK
dc.identifier.spage7490en_HK
dc.identifier.epage7498en_HK
dc.identifier.isiWOS:000251282000010-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridJin, H=24577511700en_HK
dc.identifier.scopusauthoridWang, X=7501866464en_HK
dc.identifier.scopusauthoridYing, J=12645439800en_HK
dc.identifier.scopusauthoridWong, AHY=16743208300en_HK
dc.identifier.scopusauthoridLi, H=24468545300en_HK
dc.identifier.scopusauthoridLee, KY=35080729700en_HK
dc.identifier.scopusauthoridSrivastava, G=7202242238en_HK
dc.identifier.scopusauthoridChan, ATC=13404833700en_HK
dc.identifier.scopusauthoridYeo, W=7103397662en_HK
dc.identifier.scopusauthoridMa, BBY=7403301016en_HK
dc.identifier.scopusauthoridPutti, TC=8341352700en_HK
dc.identifier.scopusauthoridLung, ML=7006411788en_HK
dc.identifier.scopusauthoridShen, ZY=7403324731en_HK
dc.identifier.scopusauthoridXu, LY=7404744339en_HK
dc.identifier.scopusauthoridLangford, C=7102621963en_HK
dc.identifier.scopusauthoridTao, Q=7102578359en_HK
dc.identifier.citeulike1373647-

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