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Article: OPCML is a broad tumor suppressor for multiple carcinomas and lymphomas with frequently epigenetic inactivation

TitleOPCML is a broad tumor suppressor for multiple carcinomas and lymphomas with frequently epigenetic inactivation
Authors
Issue Date2008
PublisherPublic Library of Science. The Journal's web site is located at http://www.plosone.org/home.action
Citation
Plos One, 2008, v. 3 n. 8 How to Cite?
Abstract
Background: Identification of tumor suppressor genes (TSGs) silenced by CpG methylation uncovers the molecular mechanism of tumorigenesis and potential tumor biomarkers. Loss of heterozygosity at 11q25 is common multiple tumors including nasopharyngeal carcinoma (NPC). OPCML, located at 11q25, is one of the downregulated genes we identified through digital expression subtraction. Methodology/Principal Findings: Semi-quantitative RT-PCR showed frequent OPCML silencing in NPC and other common tumors, with no homozygous deletion detected by multiplex differential DNA-PCR. Instead, promoter methylation of OPCML was frequently detected in multiple carcinoma cell lines (nasopharyngeal, esophageal, lung, gastric, colon, liver, breast, cervix, prostate), lymphoma cell lines (non-Hodgkin and Hodgkin lymphoma, nasal NK/T-cell lymphoma) and primary tumors, but not in any non-tumor cell line and seldom weakly methylated in normal epithelial tissues. Pharmacological and genetic demethylation restored OPCML expression, indicating a direct epigenetic silencing. We further found that OPCML is stress-responsive, but this response is epigenetically impaired when its promoter becomes methylated. Ecotopic expression of OPCML led to significant inhibition of both anchorage-dependent and -indendent growth of carcinoma cells with endogenous silencing. Conlusions/Significance: Thus, through functional epigenetics, we identified OPCML as a broad tumor suppressor, which is frequently inactivated by methylation in multiple malignancies. © 2008 Cui et al.
Persistent Identifierhttp://hdl.handle.net/10722/58183
ISSN
2013 Impact Factor: 3.534
2013 SCImago Journal Rankings: 1.724
ISI Accession Number ID
Funding AgencyGrant Number
Hong Kong RGC Central AllocationCA06/07.SC03
Chinese University of Hong Kong
Funding Information:

This project was supported by a Hong Kong RGC Central Allocation Grant (CA06/07.SC03 to QT) and a Chinese University of Hong Kong direct grant.

References

 

Author Affiliations
  1. The University of Hong Kong
  2. Yonsei University College of Medicine
  3. Johns Hopkins Singapore
  4. Uniformed Services University of the Health Sciences
  5. The Johns Hopkins School of Medicine
  6. Wyeth Laboratory, Maidenhead
  7. Peking University
  8. University of Edinburgh
  9. Chinese University of Hong Kong
DC FieldValueLanguage
dc.contributor.authorCui, Yen_HK
dc.contributor.authorYing, Yen_HK
dc.contributor.authorVan Hasselt, Aen_HK
dc.contributor.authorNg, KMen_HK
dc.contributor.authorYu, Jen_HK
dc.contributor.authorZhang, Qen_HK
dc.contributor.authorJin, Jen_HK
dc.contributor.authorLiu, Den_HK
dc.contributor.authorRhim, JSen_HK
dc.contributor.authorRha, SYen_HK
dc.contributor.authorLoyo, Men_HK
dc.contributor.authorChan, ATCen_HK
dc.contributor.authorSrivastava, Gen_HK
dc.contributor.authorTsao, GSWen_HK
dc.contributor.authorSellar, GCen_HK
dc.contributor.authorSung, JJYen_HK
dc.contributor.authorSidransky, Den_HK
dc.contributor.authorTao, Qen_HK
dc.date.accessioned2010-05-31T03:25:22Z-
dc.date.available2010-05-31T03:25:22Z-
dc.date.issued2008en_HK
dc.identifier.citationPlos One, 2008, v. 3 n. 8en_HK
dc.identifier.issn1932-6203en_HK
dc.identifier.urihttp://hdl.handle.net/10722/58183-
dc.description.abstractBackground: Identification of tumor suppressor genes (TSGs) silenced by CpG methylation uncovers the molecular mechanism of tumorigenesis and potential tumor biomarkers. Loss of heterozygosity at 11q25 is common multiple tumors including nasopharyngeal carcinoma (NPC). OPCML, located at 11q25, is one of the downregulated genes we identified through digital expression subtraction. Methodology/Principal Findings: Semi-quantitative RT-PCR showed frequent OPCML silencing in NPC and other common tumors, with no homozygous deletion detected by multiplex differential DNA-PCR. Instead, promoter methylation of OPCML was frequently detected in multiple carcinoma cell lines (nasopharyngeal, esophageal, lung, gastric, colon, liver, breast, cervix, prostate), lymphoma cell lines (non-Hodgkin and Hodgkin lymphoma, nasal NK/T-cell lymphoma) and primary tumors, but not in any non-tumor cell line and seldom weakly methylated in normal epithelial tissues. Pharmacological and genetic demethylation restored OPCML expression, indicating a direct epigenetic silencing. We further found that OPCML is stress-responsive, but this response is epigenetically impaired when its promoter becomes methylated. Ecotopic expression of OPCML led to significant inhibition of both anchorage-dependent and -indendent growth of carcinoma cells with endogenous silencing. Conlusions/Significance: Thus, through functional epigenetics, we identified OPCML as a broad tumor suppressor, which is frequently inactivated by methylation in multiple malignancies. © 2008 Cui et al.en_HK
dc.languageengen_HK
dc.publisherPublic Library of Science. The Journal's web site is located at http://www.plosone.org/home.actionen_HK
dc.relation.ispartofPLoS ONEen_HK
dc.titleOPCML is a broad tumor suppressor for multiple carcinomas and lymphomas with frequently epigenetic inactivationen_HK
dc.typeArticleen_HK
dc.identifier.emailSrivastava, G:gopesh@pathology.hku.hken_HK
dc.identifier.emailTsao, GSW:gswtsao@hkucc.hku.hken_HK
dc.identifier.authoritySrivastava, G=rp00365en_HK
dc.identifier.authorityTsao, GSW=rp00399en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1371/journal.pone.0002990en_HK
dc.identifier.pmid18714356-
dc.identifier.scopuseid_2-s2.0-52049115449en_HK
dc.identifier.hkuros150709en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-52049115449&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume3en_HK
dc.identifier.issue8en_HK
dc.identifier.isiWOS:000264420900016-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridCui, Y=55196756600en_HK
dc.identifier.scopusauthoridYing, Y=36889049800en_HK
dc.identifier.scopusauthoridVan Hasselt, A=6603932076en_HK
dc.identifier.scopusauthoridNg, KM=16053249400en_HK
dc.identifier.scopusauthoridYu, J=35351306800en_HK
dc.identifier.scopusauthoridZhang, Q=20735917800en_HK
dc.identifier.scopusauthoridJin, J=55166586700en_HK
dc.identifier.scopusauthoridLiu, D=8707626800en_HK
dc.identifier.scopusauthoridRhim, JS=35389591400en_HK
dc.identifier.scopusauthoridRha, SY=7006023235en_HK
dc.identifier.scopusauthoridLoyo, M=24068858900en_HK
dc.identifier.scopusauthoridChan, ATC=13404833700en_HK
dc.identifier.scopusauthoridSrivastava, G=7202242238en_HK
dc.identifier.scopusauthoridTsao, GSW=7102813116en_HK
dc.identifier.scopusauthoridSellar, GC=6603033630en_HK
dc.identifier.scopusauthoridSung, JJY=35405352400en_HK
dc.identifier.scopusauthoridSidransky, D=7102109701en_HK
dc.identifier.scopusauthoridTao, Q=7102578359en_HK
dc.identifier.citeulike10379631-

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