Epigenetic identification of ADAMTS18 as a novel 16q23.1 tumor suppressor frequently silenced in esophageal, nasopharyngeal and multiple other carcinomas.

Epigenetic identification of ADAMTS18 as a novel 16q23.1 tumor suppressor frequently silenced in esophageal, nasopharyngeal and multiple other carcinomas. Research Abstract Details 

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Epigenetic identification of ADAMTS18 as a novel 16q23.1 tumor suppressor frequently silenced in esophageal, nasopharyngeal and multiple other carcinomas. Abstract Text:

H Jin,X Wang,J Ying,A H Y Wong,H Li,K Y Lee,G Srivastava,A T C Chan,W Yeo,B B Y Ma,T C Putti,M L Lung,Z-Y Shen,L-Y Xu,C Langford,Q Tao,H Jin,X Wang,J Ying,A H Y Wong,H Li,K Y Lee,G Srivastava,A T C Chan,W Yeo,B B Y Ma,T C Putti,M L Lung,Z-Y Shen,L-Y Xu,C Langford,Q Tao,

Tumor 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.

Epigenetic identification of ADAMTS18 as a novel 16q23.1 tumor suppressor frequently silenced in esophageal, nasopharyngeal and multiple other carcinomas. Publishing Authors By Initials

H Jin,X Wang,J Ying,AH Wong,H Li,KY Lee,G Srivastava,AT Chan,W Yeo,BB Ma,TC Putti,ML Lung,ZY Shen,LY Xu,C Langford,Q Tao,H Jin,X Wang,J Ying,AH Wong,H Li,KY Lee,G Srivastava,AT Chan,W Yeo,BB Ma,TC Putti,ML Lung,ZY Shen,LY Xu,C Langford,Q Tao,

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Epigenetic identification of ADAMTS18 as a novel 16q23.1 tumor suppressor frequently silenced in esophageal, nasopharyngeal and multiple other carcinomas. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: Oncogene

VOLUME: 26

Page Numbers: 7490-8

Journal Abbreviation: Oncogene

ISSN: 1476-5594

DAY: 4

MONTH: 06

YEAR: 2007

Epigenetic identification of ADAMTS18 as a novel 16q23.1 tumor suppressor frequently silenced in esophageal, nasopharyngeal and multiple other carcinomas. Information

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LANGUAGE: eng

NlmUniqueID: 8711562

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Grant and Affiliation Information for Epigenetic identification of ADAMTS18 as a novel 16q23.1 tumor suppressor frequently silenced in esophageal, nasopharyngeal and multiple other carcinomas.

AFFILIATION: Cancer Epigenetics Laboratory, Sir YK Pao Center for Cancer, Department of Clinical Oncology, Hong Kong Cancer Institute, Chinese University of Hong Kong, China.

Country: England

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MEDLINETA: Oncogene

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