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Article: MAD2 expression and its significance in mitotic checkpoint control in testicular germ cell tumour

TitleMAD2 expression and its significance in mitotic checkpoint control in testicular germ cell tumour
Authors
KeywordsMAD2
Mitotic checkpoint
Testicular germ cell tumour
Issue Date2007
PublisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/bbamcr
Citation
Biochimica Et Biophysica Acta - Molecular Cell Research, 2007, v. 1773 n. 6, p. 821-832 How to Cite?
AbstractChromosomal instability (CIN) is a common characteristic in testicular germ cell tumour (TGCT). A functional mitotic checkpoint control is important for accurate chromosome segregation during mitosis. Mitotic arrest deficient 2 (MAD2) is a key component of this checkpoint and inactivation of MAD2 is correlated with checkpoint impairment. The aim of this study was to investigate the function of mitotic checkpoint control in TGCT cells and to study its association with MAD2 expression using 8 TGCT cell lines as well as 23 TGCT tissue samples. We found that in response to microtubule disruption, 6 of 8 TGCT cell lines (75%) failed to arrest in mitosis demonstrated by the decreased mitotic index and aberrant expression of mitosis regulators, indicating that mitotic checkpoint defect is a common event in TGCT cells. This loss of mitotic checkpoint control was correlated with reduced MAD2 protein expression in TGCT cell lines implicating that downregulation of MAD2 may play a critical role in an impaired mitotic checkpoint control in these cells. In addition, immunohistochemistry studies on 23 seminomas and 12 normal testis tissues demonstrated that nuclear expression of MAD2 was much lower in seminomas (p < 0.0001) but cytoplasmic MAD2 expression was higher in seminomas (p = 0.06) than normal samples. Our results suggest that aberrant MAD2 expression may play an essential role in a defective mitotic checkpoint in TGCT cells, which may contribute to CIN commonly observed in TGCT tumours. © 2007 Elsevier B.V. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/67730
ISSN
2015 Impact Factor: 5.128
2015 SCImago Journal Rankings: 3.043
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorFung, MKLen_HK
dc.contributor.authorCheung, HWen_HK
dc.contributor.authorWong, HLen_HK
dc.contributor.authorYuen, HFen_HK
dc.contributor.authorLing, MTen_HK
dc.contributor.authorChan, KWen_HK
dc.contributor.authorWong, YCen_HK
dc.contributor.authorCheung, ALMen_HK
dc.contributor.authorWang, Xen_HK
dc.date.accessioned2010-09-06T05:57:44Z-
dc.date.available2010-09-06T05:57:44Z-
dc.date.issued2007en_HK
dc.identifier.citationBiochimica Et Biophysica Acta - Molecular Cell Research, 2007, v. 1773 n. 6, p. 821-832en_HK
dc.identifier.issn0167-4889en_HK
dc.identifier.urihttp://hdl.handle.net/10722/67730-
dc.description.abstractChromosomal instability (CIN) is a common characteristic in testicular germ cell tumour (TGCT). A functional mitotic checkpoint control is important for accurate chromosome segregation during mitosis. Mitotic arrest deficient 2 (MAD2) is a key component of this checkpoint and inactivation of MAD2 is correlated with checkpoint impairment. The aim of this study was to investigate the function of mitotic checkpoint control in TGCT cells and to study its association with MAD2 expression using 8 TGCT cell lines as well as 23 TGCT tissue samples. We found that in response to microtubule disruption, 6 of 8 TGCT cell lines (75%) failed to arrest in mitosis demonstrated by the decreased mitotic index and aberrant expression of mitosis regulators, indicating that mitotic checkpoint defect is a common event in TGCT cells. This loss of mitotic checkpoint control was correlated with reduced MAD2 protein expression in TGCT cell lines implicating that downregulation of MAD2 may play a critical role in an impaired mitotic checkpoint control in these cells. In addition, immunohistochemistry studies on 23 seminomas and 12 normal testis tissues demonstrated that nuclear expression of MAD2 was much lower in seminomas (p < 0.0001) but cytoplasmic MAD2 expression was higher in seminomas (p = 0.06) than normal samples. Our results suggest that aberrant MAD2 expression may play an essential role in a defective mitotic checkpoint in TGCT cells, which may contribute to CIN commonly observed in TGCT tumours. © 2007 Elsevier B.V. All rights reserved.en_HK
dc.languageengen_HK
dc.publisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/bbamcren_HK
dc.relation.ispartofBiochimica et Biophysica Acta - Molecular Cell Researchen_HK
dc.rightsB B A - Molecular Cell Research. Copyright © Elsevier BV.en_HK
dc.subjectMAD2en_HK
dc.subjectMitotic checkpointen_HK
dc.subjectTesticular germ cell tumouren_HK
dc.subject.meshAdulten_HK
dc.subject.meshAgeden_HK
dc.subject.meshAged, 80 and overen_HK
dc.subject.meshCalcium-Binding Proteins - biosynthesisen_HK
dc.subject.meshCell Cycle Proteins - biosynthesisen_HK
dc.subject.meshCell Line, Tumoren_HK
dc.subject.meshChromosomal Instabilityen_HK
dc.subject.meshChromosome Segregationen_HK
dc.subject.meshDown-Regulationen_HK
dc.subject.meshGene Expression Regulation, Neoplasticen_HK
dc.subject.meshHumansen_HK
dc.subject.meshMaleen_HK
dc.subject.meshMiddle Ageden_HK
dc.subject.meshMitosisen_HK
dc.subject.meshNerve Tissue Proteins - biosynthesisen_HK
dc.subject.meshRepressor Proteins - biosynthesisen_HK
dc.subject.meshSeminoma - metabolism - pathologyen_HK
dc.subject.meshTesticular Neoplasms - metabolism - pathologyen_HK
dc.subject.meshTestis - metabolism - pathologyen_HK
dc.titleMAD2 expression and its significance in mitotic checkpoint control in testicular germ cell tumouren_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0167-4889&volume=1773&spage=821&epage=832&date=2007&atitle=MAD2+expression+and+its+significance+in+mitotic+checkpoint+control+in+testicular+germ+cell+tumour.en_HK
dc.identifier.emailLing, MT:patling@hkucc.hku.hken_HK
dc.identifier.emailChan, KW:hrmtckw@hku.hken_HK
dc.identifier.emailWong, YC:ycwong@hkucc.hku.hken_HK
dc.identifier.emailCheung, ALM:lmcheung@hkucc.hku.hken_HK
dc.identifier.authorityLing, MT=rp00449en_HK
dc.identifier.authorityChan, KW=rp00330en_HK
dc.identifier.authorityWong, YC=rp00316en_HK
dc.identifier.authorityCheung, ALM=rp00332en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.bbamcr.2007.03.014en_HK
dc.identifier.pmid17467818-
dc.identifier.scopuseid_2-s2.0-34249729514en_HK
dc.identifier.hkuros129045en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-34249729514&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume1773en_HK
dc.identifier.issue6en_HK
dc.identifier.spage821en_HK
dc.identifier.epage832en_HK
dc.identifier.isiWOS:000247495800015-
dc.publisher.placeNetherlandsen_HK
dc.identifier.scopusauthoridFung, MKL=8718040400en_HK
dc.identifier.scopusauthoridCheung, HW=7201839381en_HK
dc.identifier.scopusauthoridWong, HL=7402862563en_HK
dc.identifier.scopusauthoridYuen, HF=14018633400en_HK
dc.identifier.scopusauthoridLing, MT=7102229780en_HK
dc.identifier.scopusauthoridChan, KW=16444133100en_HK
dc.identifier.scopusauthoridWong, YC=7403041798en_HK
dc.identifier.scopusauthoridCheung, ALM=7401806497en_HK
dc.identifier.scopusauthoridWang, X=7501854829en_HK

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