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Article: Epigenetic inactivation of CHFR in nasopharyngeal carcinoma through promoter methylation

TitleEpigenetic inactivation of CHFR in nasopharyngeal carcinoma through promoter methylation
Authors
KeywordsCHFR
Nasopharyngeal carcinoma
Promoter hypermethylation
Issue Date2005
PublisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www.interscience.wiley.com/jpages/0899-1987/
Citation
Molecular Carcinogenesis, 2005, v. 43 n. 4, p. 237-245 How to Cite?
AbstractChromosomal instability (CIN) is a cytogenetic hallmark of human cancers. Increasing evidence suggests that impairment of mitotic checkpoint is causally associated with CIN. CHFR is one of the mitotic checkpoint regulators and it delays chromosome condensation in response to mitotic stress. Epigenetic inactivation of CHFR through promoter CpG hypermethylation may lead to CIN and has been reported in several human cancers. In this study, we investigated the CHFR gene expression in a panel of nasopharyngeal carcinoma (NPC), prostate, ovarian, and breast cancer cell lines. We found that the expression of CHFR mRNA was significantly decreased or undetectable in all eight NPC cell lines as well as three human NPC xenografts, whereas non-malignant nasopharyngeal cell lines and other cancer cell lines tested expressed CHFR at relatively high levels. Hypermethylation of CHFR promoter region was also strongly correlated with decreased CHFR expression in NPC cell lines and xenografts. Treatment with a methyltransferase inhibitor, 5-aza-2′-deoxycytidine, led to restoration of CHFR expression in NPC cell lines. More importantly, hypermethylation of CHFR promoter region was detected in 61.1% (22 out of 36) of primary NPC tumors while it was absent in non-malignant tissues. These findings suggest that downregulation of CHFR is a common event in NPC cells which may be due to hypermethylation of the gene promoter region. © 2005 Wiley-Liss, Inc.
Persistent Identifierhttp://hdl.handle.net/10722/67920
ISSN
2015 Impact Factor: 4.722
2015 SCImago Journal Rankings: 1.393
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorCheung, HWen_HK
dc.contributor.authorChing, YPen_HK
dc.contributor.authorNicholls, JMen_HK
dc.contributor.authorLing, MTen_HK
dc.contributor.authorWong, YCen_HK
dc.contributor.authorHui, Nen_HK
dc.contributor.authorCheung, Aen_HK
dc.contributor.authorTsao, SWen_HK
dc.contributor.authorWang, Qen_HK
dc.contributor.authorYeun, PWen_HK
dc.contributor.authorLo, KWen_HK
dc.contributor.authorJin, DYen_HK
dc.contributor.authorWang, Xen_HK
dc.date.accessioned2010-09-06T05:59:28Z-
dc.date.available2010-09-06T05:59:28Z-
dc.date.issued2005en_HK
dc.identifier.citationMolecular Carcinogenesis, 2005, v. 43 n. 4, p. 237-245en_HK
dc.identifier.issn0899-1987en_HK
dc.identifier.urihttp://hdl.handle.net/10722/67920-
dc.description.abstractChromosomal instability (CIN) is a cytogenetic hallmark of human cancers. Increasing evidence suggests that impairment of mitotic checkpoint is causally associated with CIN. CHFR is one of the mitotic checkpoint regulators and it delays chromosome condensation in response to mitotic stress. Epigenetic inactivation of CHFR through promoter CpG hypermethylation may lead to CIN and has been reported in several human cancers. In this study, we investigated the CHFR gene expression in a panel of nasopharyngeal carcinoma (NPC), prostate, ovarian, and breast cancer cell lines. We found that the expression of CHFR mRNA was significantly decreased or undetectable in all eight NPC cell lines as well as three human NPC xenografts, whereas non-malignant nasopharyngeal cell lines and other cancer cell lines tested expressed CHFR at relatively high levels. Hypermethylation of CHFR promoter region was also strongly correlated with decreased CHFR expression in NPC cell lines and xenografts. Treatment with a methyltransferase inhibitor, 5-aza-2′-deoxycytidine, led to restoration of CHFR expression in NPC cell lines. More importantly, hypermethylation of CHFR promoter region was detected in 61.1% (22 out of 36) of primary NPC tumors while it was absent in non-malignant tissues. These findings suggest that downregulation of CHFR is a common event in NPC cells which may be due to hypermethylation of the gene promoter region. © 2005 Wiley-Liss, Inc.en_HK
dc.languageengen_HK
dc.publisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www.interscience.wiley.com/jpages/0899-1987/en_HK
dc.relation.ispartofMolecular Carcinogenesisen_HK
dc.rightsMolecular Carcinogenesis. Copyright © John Wiley & Sons, Inc.en_HK
dc.subjectCHFRen_HK
dc.subjectNasopharyngeal carcinomaen_HK
dc.subjectPromoter hypermethylationen_HK
dc.subject.meshCell Cycle Proteins - genetics - metabolismen_HK
dc.subject.meshCell Line, Tumoren_HK
dc.subject.meshCpG Islands - geneticsen_HK
dc.subject.meshDNA Methylationen_HK
dc.subject.meshEpigenesis, Genetic - geneticsen_HK
dc.subject.meshFemaleen_HK
dc.subject.meshGene Expression Regulation, Neoplastic - geneticsen_HK
dc.subject.meshGene Silencingen_HK
dc.subject.meshHumansen_HK
dc.subject.meshMaleen_HK
dc.subject.meshNasopharyngeal Neoplasms - genetics - pathologyen_HK
dc.subject.meshNeoplasm Proteins - genetics - metabolismen_HK
dc.subject.meshPromoter Regions, Genetic - geneticsen_HK
dc.subject.meshRNA, Messenger - genetics - metabolismen_HK
dc.titleEpigenetic inactivation of CHFR in nasopharyngeal carcinoma through promoter methylationen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0899-1987&volume=43&issue=4&spage=237&epage=245&date=2005&atitle=Epigenetic+inactivation+of+CHFR+in+nasopharyngeal+carcinoma+through+promoter+methylationen_HK
dc.identifier.emailChing, YP:ypching@hku.hken_HK
dc.identifier.emailNicholls, JM:nicholls@pathology.hku.hken_HK
dc.identifier.emailLing, MT:patling@hkucc.hku.hken_HK
dc.identifier.emailWong, YC:ycwong@hkucc.hku.hken_HK
dc.identifier.emailCheung, A:lmcheung@hkucc.hku.hken_HK
dc.identifier.emailTsao, SW:gswtsao@hkucc.hku.hken_HK
dc.identifier.emailJin, DY:dyjin@hkucc.hku.hken_HK
dc.identifier.authorityChing, YP=rp00469en_HK
dc.identifier.authorityNicholls, JM=rp00364en_HK
dc.identifier.authorityLing, MT=rp00449en_HK
dc.identifier.authorityWong, YC=rp00316en_HK
dc.identifier.authorityCheung, A=rp00332en_HK
dc.identifier.authorityTsao, SW=rp00399en_HK
dc.identifier.authorityJin, DY=rp00452en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1002/mc.20106en_HK
dc.identifier.pmid15937956-
dc.identifier.scopuseid_2-s2.0-23644441130en_HK
dc.identifier.hkuros105231en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-23644441130&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume43en_HK
dc.identifier.issue4en_HK
dc.identifier.spage237en_HK
dc.identifier.epage245en_HK
dc.identifier.isiWOS:000231079900007-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridCheung, HW=7201839381en_HK
dc.identifier.scopusauthoridChing, YP=7005431277en_HK
dc.identifier.scopusauthoridNicholls, JM=7201463077en_HK
dc.identifier.scopusauthoridLing, MT=7102229780en_HK
dc.identifier.scopusauthoridWong, YC=7403041798en_HK
dc.identifier.scopusauthoridHui, N=15220645700en_HK
dc.identifier.scopusauthoridCheung, A=7401806497en_HK
dc.identifier.scopusauthoridTsao, SW=7102813116en_HK
dc.identifier.scopusauthoridWang, Q=7406910452en_HK
dc.identifier.scopusauthoridYeun, PW=15221849400en_HK
dc.identifier.scopusauthoridLo, KW=7402101603en_HK
dc.identifier.scopusauthoridJin, DY=7201973614en_HK
dc.identifier.scopusauthoridWang, X=7501854829en_HK

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