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Article: CMTM3, located at the critical tumor suppressor locus 16q22.1, is silenced by CpG methylation in carcinomas and inhibits tumor cell growth through inducing apoptosis

TitleCMTM3, located at the critical tumor suppressor locus 16q22.1, is silenced by CpG methylation in carcinomas and inhibits tumor cell growth through inducing apoptosis
Authors
Issue Date2009
PublisherAmerican Association for Cancer Research. The Journal's web site is located at http://cancerres.aacrjournals.org/
Citation
Cancer Research, 2009, v. 69 n. 12, p. 5194-5201 How to Cite?
AbstractClosely located at the tumor suppressor locus 16q22.1, CKLF-like MARVEL transmembrane domain-containing member 3 and 4 (CMTM3 and CMTM4) encode two CMTM family proteins, which link chemokines and the transmembrane-4 superfamily. In contrast to the broad expression of both CMTM3 and CMTM4 in normal human adult tissues, only CMTM3 is silenced or down-regulated in common carcinoma (gastric, breast, nasopharyngeal, esophageal, and colon) cell lines and primary tumors. CMTM3 methylation was not detected in normal epithelial cell lines and tissues, with weak methylation present in only 5 of 35 (14%) gastric cancer adjacent normal tissues. Furthermore, immunohistochemistry showed that CMTM3 protein was absent in 12 of 35 (34%) gastric and 1 of 2 colorectal tumors, which was well correlated with its methylation status. The silencing of CMTM3 is due to aberrant promoter CpG methylation that could be reversed by pharmacologic demethylation. Ectopic expression of CMTM3 strongly suppressed the colony formation of carcinoma cell lines. In addition, CMTM3 inhibited tumor cell growth and induced apoptosis with caspase-3 activation. Thus, CMTM3 exerts tumor-suppressive functions in tumor cells, with frequent epigenetic inactivation by promoter CpG methylation in common carcinomas. ©2009 American Association for Cancer Research.
Persistent Identifierhttp://hdl.handle.net/10722/148603
ISSN
2015 Impact Factor: 8.556
2015 SCImago Journal Rankings: 5.372
ISI Accession Number ID
Funding AgencyGrant Number
New Century Excellent Talents in UniversityNCET-07-0013
China High Tech 863 Program2006AA02A305
Michael and Betty Kadoorie Cancer Genetics Research Program
Hong Kong RGC Central AllocationCA06/07.SC03
Funding Information:

Program for New Century Excellent Talents in University grant NCET-07-0013, China High Tech 863 Program grant 2006AA02A305, and Michael and Betty Kadoorie Cancer Genetics Research Program grant MBKCGRP and Hong Kong RGC Central Allocation Grant CA06/07.SC03 (Q. Tao).

References

 

DC FieldValueLanguage
dc.contributor.authorWang, Yen_US
dc.contributor.authorLi, Jen_US
dc.contributor.authorCui, Yen_US
dc.contributor.authorLi, Ten_US
dc.contributor.authorKa, MNen_US
dc.contributor.authorGeng, Hen_US
dc.contributor.authorLi, Hen_US
dc.contributor.authorShu, XSen_US
dc.contributor.authorLi, Hen_US
dc.contributor.authorLiu, Wen_US
dc.contributor.authorLuo, Ben_US
dc.contributor.authorZhang, Qen_US
dc.contributor.authorMok, TSKen_US
dc.contributor.authorZheng, Wen_US
dc.contributor.authorQiu, Xen_US
dc.contributor.authorSrivastava, Gen_US
dc.contributor.authorYu, Jen_US
dc.contributor.authorSung, JJYen_US
dc.contributor.authorChan, ATCen_US
dc.contributor.authorMa, Den_US
dc.contributor.authorTao, Qen_US
dc.contributor.authorHan, Wen_US
dc.date.accessioned2012-05-29T06:14:02Z-
dc.date.available2012-05-29T06:14:02Z-
dc.date.issued2009en_US
dc.identifier.citationCancer Research, 2009, v. 69 n. 12, p. 5194-5201en_US
dc.identifier.issn0008-5472en_US
dc.identifier.urihttp://hdl.handle.net/10722/148603-
dc.description.abstractClosely located at the tumor suppressor locus 16q22.1, CKLF-like MARVEL transmembrane domain-containing member 3 and 4 (CMTM3 and CMTM4) encode two CMTM family proteins, which link chemokines and the transmembrane-4 superfamily. In contrast to the broad expression of both CMTM3 and CMTM4 in normal human adult tissues, only CMTM3 is silenced or down-regulated in common carcinoma (gastric, breast, nasopharyngeal, esophageal, and colon) cell lines and primary tumors. CMTM3 methylation was not detected in normal epithelial cell lines and tissues, with weak methylation present in only 5 of 35 (14%) gastric cancer adjacent normal tissues. Furthermore, immunohistochemistry showed that CMTM3 protein was absent in 12 of 35 (34%) gastric and 1 of 2 colorectal tumors, which was well correlated with its methylation status. The silencing of CMTM3 is due to aberrant promoter CpG methylation that could be reversed by pharmacologic demethylation. Ectopic expression of CMTM3 strongly suppressed the colony formation of carcinoma cell lines. In addition, CMTM3 inhibited tumor cell growth and induced apoptosis with caspase-3 activation. Thus, CMTM3 exerts tumor-suppressive functions in tumor cells, with frequent epigenetic inactivation by promoter CpG methylation in common carcinomas. ©2009 American Association for Cancer Research.en_US
dc.languageengen_US
dc.publisherAmerican Association for Cancer Research. The Journal's web site is located at http://cancerres.aacrjournals.org/en_US
dc.relation.ispartofCancer Researchen_US
dc.subject.meshApoptosis - Geneticsen_US
dc.subject.meshBase Sequenceen_US
dc.subject.meshCell Division - Geneticsen_US
dc.subject.meshCell Line, Tumoren_US
dc.subject.meshChemokines - Geneticsen_US
dc.subject.meshChromosomes, Human, Pair 16en_US
dc.subject.meshCpg Islandsen_US
dc.subject.meshDna Methylationen_US
dc.subject.meshDna Primersen_US
dc.subject.meshFlow Cytometryen_US
dc.subject.meshGene Silencingen_US
dc.subject.meshHumansen_US
dc.subject.meshImmunohistochemistryen_US
dc.subject.meshMembrane Proteins - Geneticsen_US
dc.subject.meshNeoplasms - Genetics - Pathologyen_US
dc.subject.meshReverse Transcriptase Polymerase Chain Reactionen_US
dc.titleCMTM3, located at the critical tumor suppressor locus 16q22.1, is silenced by CpG methylation in carcinomas and inhibits tumor cell growth through inducing apoptosisen_US
dc.typeArticleen_US
dc.identifier.emailSrivastava, G:gopesh@pathology.hku.hken_US
dc.identifier.authoritySrivastava, G=rp00365en_US
dc.description.naturelink_to_OA_fulltexten_US
dc.identifier.doi10.1158/0008-5472.CAN-08-3694en_US
dc.identifier.pmid19509237-
dc.identifier.scopuseid_2-s2.0-67449127092en_US
dc.identifier.hkuros167069-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-67449127092&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume69en_US
dc.identifier.issue12en_US
dc.identifier.spage5194en_US
dc.identifier.epage5201en_US
dc.identifier.isiWOS:000267506400035-
dc.publisher.placeUnited Statesen_US

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