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Article: Id-1 promotes chromosomal instability through modification of APC/C activity during mitosis in response to microtubule disruption

TitleId-1 promotes chromosomal instability through modification of APC/C activity during mitosis in response to microtubule disruption
Authors
Issue Date2008
PublisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/onc
Citation
Oncogene, 2008, v. 27 n. 32, p. 4456-4466 How to Cite?
AbstractId-1 (Inhibitor of DNA binding/differential-1) plays a positive role in tumorigenesis through regulation of multiple signaling pathways. Recently, it is suggested that upregulation of Id-1 in cancer cells promotes chromosomal instability. However, the underlying molecular mechanism is not known. In this study, we report a novel function of Id-1 in regulation of mitosis through physical interaction with Cdc20 (cell division cycle protein 20) and Cdh1 (Cdc20 homolog 1). During early mitosis, Id-1 interacts with Cdc20 and RASSF1A (Ras association domain family 1A), leading to enhanced APCCdc20 activity, which in turn promotes cyclin B1/securin degradation and premature mitosis. During late mitosis, Id-1 binds to Cdh1 and disrupts the interaction between Cdh1 and APC, resulting in suppression of APCCdh1 activity. On the other hand, overexpression of Cdh1 leads to Id-1 protein degradation, suggesting that Id-1 may also act as a substrate of APCCdh1. The negative effect of Id-1 on APCCdh1 results in suppression of APC Cdh1-induced Aurora A and Cdc20 degradation, leading to failure in cytokinesis. As a result, overexpression of Id-1 in human prostate epithelial cells leads to polyploidy in response to microtubule disruption, and this effect is abolished when Id-1 expression is suppressed using antisense technology. These results demonstrate a novel function of Id-1 in promoting chromosomal instability through modification of APC/C activity during mitosis and provide a novel molecular mechanism accounted for the function of Id-1 as an oncogene. © 2008 Macmillan Publishers Limited All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/149700
ISSN
2015 Impact Factor: 7.932
2015 SCImago Journal Rankings: 4.047
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorWang, Xen_US
dc.contributor.authorDi, Ken_US
dc.contributor.authorZhang, Xen_US
dc.contributor.authorHan, HYen_US
dc.contributor.authorWong, YCen_US
dc.contributor.authorLeung, SCLen_US
dc.contributor.authorLing, MTen_US
dc.date.accessioned2012-06-26T05:57:19Z-
dc.date.available2012-06-26T05:57:19Z-
dc.date.issued2008en_US
dc.identifier.citationOncogene, 2008, v. 27 n. 32, p. 4456-4466en_US
dc.identifier.issn0950-9232en_US
dc.identifier.urihttp://hdl.handle.net/10722/149700-
dc.description.abstractId-1 (Inhibitor of DNA binding/differential-1) plays a positive role in tumorigenesis through regulation of multiple signaling pathways. Recently, it is suggested that upregulation of Id-1 in cancer cells promotes chromosomal instability. However, the underlying molecular mechanism is not known. In this study, we report a novel function of Id-1 in regulation of mitosis through physical interaction with Cdc20 (cell division cycle protein 20) and Cdh1 (Cdc20 homolog 1). During early mitosis, Id-1 interacts with Cdc20 and RASSF1A (Ras association domain family 1A), leading to enhanced APCCdc20 activity, which in turn promotes cyclin B1/securin degradation and premature mitosis. During late mitosis, Id-1 binds to Cdh1 and disrupts the interaction between Cdh1 and APC, resulting in suppression of APCCdh1 activity. On the other hand, overexpression of Cdh1 leads to Id-1 protein degradation, suggesting that Id-1 may also act as a substrate of APCCdh1. The negative effect of Id-1 on APCCdh1 results in suppression of APC Cdh1-induced Aurora A and Cdc20 degradation, leading to failure in cytokinesis. As a result, overexpression of Id-1 in human prostate epithelial cells leads to polyploidy in response to microtubule disruption, and this effect is abolished when Id-1 expression is suppressed using antisense technology. These results demonstrate a novel function of Id-1 in promoting chromosomal instability through modification of APC/C activity during mitosis and provide a novel molecular mechanism accounted for the function of Id-1 as an oncogene. © 2008 Macmillan Publishers Limited All rights reserved.en_US
dc.languageengen_US
dc.publisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/oncen_US
dc.relation.ispartofOncogeneen_US
dc.subject.meshCell Cycle Proteins - Physiologyen_US
dc.subject.meshCell Lineen_US
dc.subject.meshChromosomal Instabilityen_US
dc.subject.meshCyclin B - Metabolismen_US
dc.subject.meshCyclin B1en_US
dc.subject.meshG1 Phaseen_US
dc.subject.meshHumansen_US
dc.subject.meshInhibitor Of Differentiation Protein 1 - Physiologyen_US
dc.subject.meshMicrotubules - Physiologyen_US
dc.subject.meshMitosisen_US
dc.subject.meshProtein-Serine-Threonine Kinases - Metabolismen_US
dc.subject.meshTumor Suppressor Proteins - Physiologyen_US
dc.subject.meshUbiquitin - Metabolismen_US
dc.subject.meshUbiquitin-Protein Ligase Complexes - Physiologyen_US
dc.titleId-1 promotes chromosomal instability through modification of APC/C activity during mitosis in response to microtubule disruptionen_US
dc.typeArticleen_US
dc.identifier.emailWong, YC:ycwong@hkucc.hku.hken_US
dc.identifier.emailLing, MT:patling@hkucc.hku.hken_US
dc.identifier.authorityWong, YC=rp00316en_US
dc.identifier.authorityLing, MT=rp00449en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1038/onc.2008.87en_US
dc.identifier.pmid18372912-
dc.identifier.scopuseid_2-s2.0-47949101916en_US
dc.identifier.hkuros147325-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-47949101916&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume27en_US
dc.identifier.issue32en_US
dc.identifier.spage4456en_US
dc.identifier.epage4466en_US
dc.identifier.isiWOS:000257881700008-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridWang, X=7501854829en_US
dc.identifier.scopusauthoridDi, K=14526710900en_US
dc.identifier.scopusauthoridZhang, X=8299216200en_US
dc.identifier.scopusauthoridHan, HY=24477301600en_US
dc.identifier.scopusauthoridWong, YC=7403041798en_US
dc.identifier.scopusauthoridLeung, SCL=36894169100en_US
dc.identifier.scopusauthoridLing, MT=7102229780en_US
dc.identifier.citeulike2616864-

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