File Download
There are no files associated with this item.
Links for fulltext
(May Require Subscription)
- Publisher Website: 10.1038/onc.2008.87
- Scopus: eid_2-s2.0-47949101916
- PMID: 18372912
- WOS: WOS:000257881700008
- Find via
Supplementary
- Citations:
- Appears in Collections:
Article: Id-1 promotes chromosomal instability through modification of APC/C activity during mitosis in response to microtubule disruption
Title | Id-1 promotes chromosomal instability through modification of APC/C activity during mitosis in response to microtubule disruption |
---|---|
Authors | |
Keywords | Aneuploidy Cdc20 Cdh1 Id-1 Mitosis |
Issue Date | 2008 |
Publisher | Nature 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? |
Abstract | Id-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 Identifier | http://hdl.handle.net/10722/149700 |
ISSN | 2023 Impact Factor: 6.9 2023 SCImago Journal Rankings: 2.334 |
ISI Accession Number ID | |
References |
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Wang, X | en_US |
dc.contributor.author | Di, K | en_US |
dc.contributor.author | Zhang, X | en_US |
dc.contributor.author | Han, HY | en_US |
dc.contributor.author | Wong, YC | en_US |
dc.contributor.author | Leung, SCL | en_US |
dc.contributor.author | Ling, MT | en_US |
dc.date.accessioned | 2012-06-26T05:57:19Z | - |
dc.date.available | 2012-06-26T05:57:19Z | - |
dc.date.issued | 2008 | en_US |
dc.identifier.citation | Oncogene, 2008, v. 27 n. 32, p. 4456-4466 | en_US |
dc.identifier.issn | 0950-9232 | en_US |
dc.identifier.uri | http://hdl.handle.net/10722/149700 | - |
dc.description.abstract | Id-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.language | eng | en_US |
dc.publisher | Nature Publishing Group. The Journal's web site is located at http://www.nature.com/onc | en_US |
dc.relation.ispartof | Oncogene | en_US |
dc.subject | Aneuploidy | - |
dc.subject | Cdc20 | - |
dc.subject | Cdh1 | - |
dc.subject | Id-1 | - |
dc.subject | Mitosis | - |
dc.subject.mesh | Cell Cycle Proteins - Physiology | en_US |
dc.subject.mesh | Cell Line | en_US |
dc.subject.mesh | Chromosomal Instability | en_US |
dc.subject.mesh | Cyclin B - Metabolism | en_US |
dc.subject.mesh | Cyclin B1 | en_US |
dc.subject.mesh | G1 Phase | en_US |
dc.subject.mesh | Humans | en_US |
dc.subject.mesh | Inhibitor Of Differentiation Protein 1 - Physiology | en_US |
dc.subject.mesh | Microtubules - Physiology | en_US |
dc.subject.mesh | Mitosis | en_US |
dc.subject.mesh | Protein-Serine-Threonine Kinases - Metabolism | en_US |
dc.subject.mesh | Tumor Suppressor Proteins - Physiology | en_US |
dc.subject.mesh | Ubiquitin - Metabolism | en_US |
dc.subject.mesh | Ubiquitin-Protein Ligase Complexes - Physiology | en_US |
dc.title | Id-1 promotes chromosomal instability through modification of APC/C activity during mitosis in response to microtubule disruption | en_US |
dc.type | Article | en_US |
dc.identifier.email | Wong, YC:ycwong@hkucc.hku.hk | en_US |
dc.identifier.email | Ling, MT:patling@hkucc.hku.hk | en_US |
dc.identifier.authority | Wong, YC=rp00316 | en_US |
dc.identifier.authority | Ling, MT=rp00449 | en_US |
dc.description.nature | link_to_subscribed_fulltext | en_US |
dc.identifier.doi | 10.1038/onc.2008.87 | en_US |
dc.identifier.pmid | 18372912 | - |
dc.identifier.scopus | eid_2-s2.0-47949101916 | en_US |
dc.identifier.hkuros | 147325 | - |
dc.relation.references | http://www.scopus.com/mlt/select.url?eid=2-s2.0-47949101916&selection=ref&src=s&origin=recordpage | en_US |
dc.identifier.volume | 27 | en_US |
dc.identifier.issue | 32 | en_US |
dc.identifier.spage | 4456 | en_US |
dc.identifier.epage | 4466 | en_US |
dc.identifier.isi | WOS:000257881700008 | - |
dc.publisher.place | United Kingdom | en_US |
dc.identifier.scopusauthorid | Wang, X=7501854829 | en_US |
dc.identifier.scopusauthorid | Di, K=14526710900 | en_US |
dc.identifier.scopusauthorid | Zhang, X=8299216200 | en_US |
dc.identifier.scopusauthorid | Han, HY=24477301600 | en_US |
dc.identifier.scopusauthorid | Wong, YC=7403041798 | en_US |
dc.identifier.scopusauthorid | Leung, SCL=36894169100 | en_US |
dc.identifier.scopusauthorid | Ling, MT=7102229780 | en_US |
dc.identifier.citeulike | 2616864 | - |
dc.identifier.issnl | 0950-9232 | - |