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Article: p21/Cyclin E pathway modulates anticlastogenic function of Bmi-1 in cancer cells.

Titlep21/Cyclin E pathway modulates anticlastogenic function of Bmi-1 in cancer cells.
Authors
Issue Date2015
PublisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/journal/29331/home
Citation
International Journal of Cancer, 2015, v. 136 n. 6, p. 1361-1370 How to Cite?
AbstractApart from regulating stem cell self-renewal, embryonic development and proliferation, Bmi-1 has been recently reported to be critical in the maintenance of genome integrity. In searching for novel mechanisms underlying the anticlastogenic function of Bmi-1, we observed, for the first time, that Bmi-1 positively regulates p21 expression. We extended the finding that Bmi-1 deficiency induced chromosome breaks in multiple cancer cell models. Interestingly, we further demonstrated that knockdown of cyclin E or ectopic overexpression of p21 rescued Bmi-1 deficiency-induced chromosome breaks. We therefore conclude that p21/cyclin E pathway is crucial in modulating the anticlastogenic function of Bmi-1. As it is well established that the overexpression of cyclin E potently induces genome instability and p21 suppresses the function of cyclin E, the novel and important implication from our findings is that Bmi-1 plays an important role in limiting genomic instability in cylin E-overexpressing cancer cells by positive regulation of p21.
Persistent Identifierhttp://hdl.handle.net/10722/210681
ISSN
2015 Impact Factor: 5.531
2015 SCImago Journal Rankings: 2.657
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorDeng, W-
dc.contributor.authorZHOU, Y-
dc.contributor.authorTiwari, AFY-
dc.contributor.authorSu, H-
dc.contributor.authorYang, J-
dc.contributor.authorZHU, D-
dc.contributor.authorLAU, MY-
dc.contributor.authorHau, PM-
dc.contributor.authorYip, YL-
dc.contributor.authorCheung, A-
dc.contributor.authorGuan, X-
dc.contributor.authorTsao, GSW-
dc.date.accessioned2015-06-23T05:46:12Z-
dc.date.available2015-06-23T05:46:12Z-
dc.date.issued2015-
dc.identifier.citationInternational Journal of Cancer, 2015, v. 136 n. 6, p. 1361-1370-
dc.identifier.issn0020-7136-
dc.identifier.urihttp://hdl.handle.net/10722/210681-
dc.description.abstractApart from regulating stem cell self-renewal, embryonic development and proliferation, Bmi-1 has been recently reported to be critical in the maintenance of genome integrity. In searching for novel mechanisms underlying the anticlastogenic function of Bmi-1, we observed, for the first time, that Bmi-1 positively regulates p21 expression. We extended the finding that Bmi-1 deficiency induced chromosome breaks in multiple cancer cell models. Interestingly, we further demonstrated that knockdown of cyclin E or ectopic overexpression of p21 rescued Bmi-1 deficiency-induced chromosome breaks. We therefore conclude that p21/cyclin E pathway is crucial in modulating the anticlastogenic function of Bmi-1. As it is well established that the overexpression of cyclin E potently induces genome instability and p21 suppresses the function of cyclin E, the novel and important implication from our findings is that Bmi-1 plays an important role in limiting genomic instability in cylin E-overexpressing cancer cells by positive regulation of p21.-
dc.languageeng-
dc.publisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/journal/29331/home-
dc.relation.ispartofInternational Journal of Cancer-
dc.rightsInternational Journal of Cancer. Copyright © John Wiley & Sons, Inc.-
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.titlep21/Cyclin E pathway modulates anticlastogenic function of Bmi-1 in cancer cells.-
dc.typeArticle-
dc.identifier.emailDeng, W: wdeng@hkucc.hku.hk-
dc.identifier.emailTiwari, AFY: tiwari@hku.hk-
dc.identifier.emailYang, J: jiesarah@hku.hk-
dc.identifier.emailHau, PM: tomhau10@hku.hk-
dc.identifier.emailYip, YL: yimling@hkucc.hku.hk-
dc.identifier.emailCheung, A: lmcheung@hku.hk-
dc.identifier.emailGuan, X: xyguan@hkucc.hku.hk-
dc.identifier.emailTsao, GSW: gswtsao@hku.hk-
dc.identifier.authorityDeng, W=rp01640-
dc.identifier.authorityTiwari, AFY=rp00441-
dc.identifier.authorityCheung, A=rp00332-
dc.identifier.authorityGuan, X=rp00454-
dc.identifier.authorityTsao, GSW=rp00399-
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1002/ijc.29114-
dc.identifier.pmid25131797-
dc.identifier.pmcidPMC4312942-
dc.identifier.scopuseid_2-s2.0-84922258287-
dc.identifier.hkuros243631-
dc.identifier.volume136-
dc.identifier.issue6-
dc.identifier.spage1361-
dc.identifier.epage1370-
dc.identifier.isiWOS:000347705200042-
dc.publisher.placeUnited States-

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