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Aurora-A kinase inhibition enhances the cytosine arabinoside-induced cell death in leukemia cells through apoptosis and mitotic catastrophe

DC FieldValueLanguage
dc.contributor.author김수정-
dc.contributor.author민유홍-
dc.contributor.author엄주인-
dc.contributor.author정준원-
dc.contributor.author정회경-
dc.date.accessioned2015-04-23T17:01:33Z-
dc.date.available2015-04-23T17:01:33Z-
dc.date.issued2010-
dc.identifier.issn0304-3835-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/101682-
dc.description.abstractAurora-A (Aur-A) is a centrosome-associated serine/threonine kinase that is overexpressed in various cancers and potentially correlated with chemoresistance. In the Ara-C-sensitive leukemia cell lines, silencing of Aur-A by small interfering RNA transfection led to a significant increase in the Ara-C-induced cell death rate through induction of mitochondria-mediated, caspase-dependent apoptosis. In contrast, combined treatment of the Ara-C-resistant leukemia cell lines with Aur-A siRNA and Ara-C remarkably enhanced the cell death rate via non-caspase-dependent mitotic catastrophe. Taken together, Aur-A inhibition was an effective treatment for both the Ara-C-sensitive and resistant leukemia cells by increasing apoptosis and mitotic catastrophe, respectively.-
dc.description.statementOfResponsibilityopen-
dc.format.extent171~181-
dc.relation.isPartOfCancer Letters-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.titleAurora-A kinase inhibition enhances the cytosine arabinoside-induced cell death in leukemia cells through apoptosis and mitotic catastrophe-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Internal Medicine (내과학)-
dc.contributor.googleauthorJune-Won Cheong-
dc.contributor.googleauthorHaeng-Im Jung-
dc.contributor.googleauthorJu In Eom-
dc.contributor.googleauthorSoo Jung Kim-
dc.contributor.googleauthorHoi-Kyung Jeung-
dc.contributor.googleauthorYoo Hong Min-
dc.identifier.doi10.1016/j.canlet.2010.05.009-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA00633-
dc.contributor.localIdA01407-
dc.contributor.localIdA02338-
dc.contributor.localIdA03729-
dc.contributor.localIdA03787-
dc.relation.journalcodeJ00448-
dc.identifier.urlhttp://www.sciencedirect.com/science/article/pii/S0304383510002855-
dc.contributor.alternativeNameKim, Soo Jeong-
dc.contributor.alternativeNameMin, Yoo Hong-
dc.contributor.alternativeNameEom, Ju In-
dc.contributor.alternativeNameCheong, June Won-
dc.contributor.alternativeNameJeung, Hoi Kyung-
dc.contributor.affiliatedAuthorKim, Soo Jeong-
dc.contributor.affiliatedAuthorMin, Yoo Hong-
dc.contributor.affiliatedAuthorEom, Ju In-
dc.contributor.affiliatedAuthorCheong, June-Won-
dc.contributor.affiliatedAuthorJeung, Hoi Kyung-
dc.citation.volume297-
dc.citation.number2-
dc.citation.startPage171-
dc.citation.endPage181-
dc.identifier.bibliographicCitationCancer Letters, Vol.297(2) : 171-181, 2010-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Internal Medicine (내과학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Yonsei Biomedical Research Center (연세의생명연구원) > 1. Journal Papers

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