Aurora-A kinase inhibition enhances the cytosine arabinoside-induced cell death in leukemia cells through apoptosis and mitotic catastrophe
Abstract Aurora-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...
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| Veröffentlicht in: | Cancer letters 2010-11, Vol.297 (2), p.171-181 |
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| container_title | Cancer letters |
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| creator | Cheong, June-Won Jung, Haeng-Im Eom, Ju In Kim, Soo Jung Jeung, Hoi-Kyung Min, Yoo Hong |
| description | Abstract Aurora-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. |
| doi_str_mv | 10.1016/j.canlet.2010.05.009 |
| format | Article |
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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.</description><identifier>ISSN: 0304-3835</identifier><identifier>EISSN: 1872-7980</identifier><identifier>DOI: 10.1016/j.canlet.2010.05.009</identifier><identifier>PMID: 20547440</identifier><language>eng</language><publisher>Ireland: Elsevier Ireland Ltd</publisher><subject>Acute leukemia ; Apoptosis ; Apoptosis - drug effects ; Ara-C ; Aurora kinase ; Aurora Kinases ; Caspases - metabolism ; Cell cycle ; Cell Cycle - drug effects ; Cell Death - drug effects ; Cell Line, Tumor ; Cell Survival ; Chemotherapy ; Cytarabine - pharmacology ; Hematology, Oncology and Palliative Medicine ; HL-60 Cells ; Humans ; Kinases ; Leukemia ; Leukemia, Myeloid, Acute - drug therapy ; Leukemia, Myeloid, Acute - enzymology ; Leukemia, Myeloid, Acute - pathology ; Leukemia, Myeloid, Acute - therapy ; Membrane Potential, Mitochondrial - drug effects ; Mitochondria - drug effects ; Mitochondria - genetics ; Mitochondria - metabolism ; Mitosis - drug effects ; Mitotic catastrophe ; p38 Mitogen-Activated Protein Kinases - metabolism ; Protein-Serine-Threonine Kinases - antagonists & inhibitors ; Protein-Serine-Threonine Kinases - genetics ; RNA, Small Interfering - administration & dosage ; RNA, Small Interfering - genetics ; Transfection</subject><ispartof>Cancer letters, 2010-11, Vol.297 (2), p.171-181</ispartof><rights>Elsevier Ireland Ltd</rights><rights>2010 Elsevier Ireland Ltd</rights><rights>Copyright © 2010 Elsevier Ireland Ltd. All rights reserved.</rights><rights>Copyright Elsevier Limited Nov 28, 2010</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c444t-602eb3952c011864f6e2c99febb176a641ae9a236de2f8eba5be6f9eb03ba6ba3</citedby><cites>FETCH-LOGICAL-c444t-602eb3952c011864f6e2c99febb176a641ae9a236de2f8eba5be6f9eb03ba6ba3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.canlet.2010.05.009$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>315,781,785,3551,27929,27930,46000</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20547440$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Cheong, June-Won</creatorcontrib><creatorcontrib>Jung, Haeng-Im</creatorcontrib><creatorcontrib>Eom, Ju In</creatorcontrib><creatorcontrib>Kim, Soo Jung</creatorcontrib><creatorcontrib>Jeung, Hoi-Kyung</creatorcontrib><creatorcontrib>Min, Yoo Hong</creatorcontrib><title>Aurora-A kinase inhibition enhances the cytosine arabinoside-induced cell death in leukemia cells through apoptosis and mitotic catastrophe</title><title>Cancer letters</title><addtitle>Cancer Lett</addtitle><description>Abstract Aurora-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.</description><subject>Acute leukemia</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Ara-C</subject><subject>Aurora kinase</subject><subject>Aurora Kinases</subject><subject>Caspases - metabolism</subject><subject>Cell cycle</subject><subject>Cell Cycle - drug effects</subject><subject>Cell Death - drug effects</subject><subject>Cell Line, Tumor</subject><subject>Cell Survival</subject><subject>Chemotherapy</subject><subject>Cytarabine - pharmacology</subject><subject>Hematology, Oncology and Palliative Medicine</subject><subject>HL-60 Cells</subject><subject>Humans</subject><subject>Kinases</subject><subject>Leukemia</subject><subject>Leukemia, Myeloid, Acute - drug therapy</subject><subject>Leukemia, Myeloid, Acute - enzymology</subject><subject>Leukemia, Myeloid, Acute - pathology</subject><subject>Leukemia, Myeloid, Acute - therapy</subject><subject>Membrane Potential, Mitochondrial - drug effects</subject><subject>Mitochondria - drug effects</subject><subject>Mitochondria - genetics</subject><subject>Mitochondria - metabolism</subject><subject>Mitosis - drug effects</subject><subject>Mitotic catastrophe</subject><subject>p38 Mitogen-Activated Protein Kinases - metabolism</subject><subject>Protein-Serine-Threonine Kinases - antagonists & inhibitors</subject><subject>Protein-Serine-Threonine Kinases - genetics</subject><subject>RNA, Small Interfering - administration & dosage</subject><subject>RNA, Small Interfering - genetics</subject><subject>Transfection</subject><issn>0304-3835</issn><issn>1872-7980</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFUk2LFDEQbURx19V_IBLw3GMl3cl0X4Rh8QsWPKjnUElX25npScYkLcxv8E-bdlYFL56qKN57xatXVfWcw4YDV6_2G4t-prwRUEYgNwD9g-qad1tRb_sOHlbX0EBbN10jr6onKe0BQLZb-bi6EmvTtnBd_dgtMUSsd-zgPCZizk_OuOyCZ-Qn9JYSyxMxe84hOU8MIxrnSz9Q7fywWBqYpXlmA2GeCp_NtBzo6PDXeGXHsHydGJ7CadVIDP3Aji6H7CyzmDHlGE4TPa0ejTgnenZfb6ovb998vn1f33189-F2d1fbtm1zrUCQaXopLHDeqXZUJGzfj2QM3ypULUfqUTRqIDF2ZFAaUmNPBhqDymBzU7286J5i-LZQynoflujLSs0lKJBKim1BtReUjSGlSKM-RXfEeNYc9JqA3utLAnpNQIPUJYFCe3EvvpgjDX9Iv09eAK8vACoWvzuKOllH5c6Di2SzHoL734Z_BezsvLM4H-hM6a8XnYQG_Wn9gvUJeMlfdFI2PwHkJrFO</recordid><startdate>20101128</startdate><enddate>20101128</enddate><creator>Cheong, June-Won</creator><creator>Jung, Haeng-Im</creator><creator>Eom, Ju In</creator><creator>Kim, Soo Jung</creator><creator>Jeung, Hoi-Kyung</creator><creator>Min, Yoo Hong</creator><general>Elsevier Ireland Ltd</general><general>Elsevier Limited</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7TO</scope><scope>7U9</scope><scope>H94</scope><scope>K9.</scope><scope>NAPCQ</scope></search><sort><creationdate>20101128</creationdate><title>Aurora-A kinase inhibition enhances the cytosine arabinoside-induced cell death in leukemia cells through apoptosis and mitotic catastrophe</title><author>Cheong, June-Won ; Jung, Haeng-Im ; Eom, Ju In ; Kim, Soo Jung ; Jeung, Hoi-Kyung ; Min, Yoo Hong</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c444t-602eb3952c011864f6e2c99febb176a641ae9a236de2f8eba5be6f9eb03ba6ba3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Acute leukemia</topic><topic>Apoptosis</topic><topic>Apoptosis - drug effects</topic><topic>Ara-C</topic><topic>Aurora kinase</topic><topic>Aurora Kinases</topic><topic>Caspases - metabolism</topic><topic>Cell cycle</topic><topic>Cell Cycle - drug effects</topic><topic>Cell Death - drug effects</topic><topic>Cell Line, Tumor</topic><topic>Cell Survival</topic><topic>Chemotherapy</topic><topic>Cytarabine - pharmacology</topic><topic>Hematology, Oncology and Palliative Medicine</topic><topic>HL-60 Cells</topic><topic>Humans</topic><topic>Kinases</topic><topic>Leukemia</topic><topic>Leukemia, Myeloid, Acute - drug therapy</topic><topic>Leukemia, Myeloid, Acute - enzymology</topic><topic>Leukemia, Myeloid, Acute - pathology</topic><topic>Leukemia, Myeloid, Acute - therapy</topic><topic>Membrane Potential, Mitochondrial - drug effects</topic><topic>Mitochondria - drug effects</topic><topic>Mitochondria - genetics</topic><topic>Mitochondria - metabolism</topic><topic>Mitosis - drug effects</topic><topic>Mitotic catastrophe</topic><topic>p38 Mitogen-Activated Protein Kinases - metabolism</topic><topic>Protein-Serine-Threonine Kinases - antagonists & inhibitors</topic><topic>Protein-Serine-Threonine Kinases - genetics</topic><topic>RNA, Small Interfering - administration & dosage</topic><topic>RNA, Small Interfering - genetics</topic><topic>Transfection</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Cheong, June-Won</creatorcontrib><creatorcontrib>Jung, Haeng-Im</creatorcontrib><creatorcontrib>Eom, Ju In</creatorcontrib><creatorcontrib>Kim, Soo Jung</creatorcontrib><creatorcontrib>Jeung, Hoi-Kyung</creatorcontrib><creatorcontrib>Min, Yoo Hong</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><jtitle>Cancer letters</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Cheong, June-Won</au><au>Jung, Haeng-Im</au><au>Eom, Ju In</au><au>Kim, Soo Jung</au><au>Jeung, Hoi-Kyung</au><au>Min, Yoo Hong</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Aurora-A kinase inhibition enhances the cytosine arabinoside-induced cell death in leukemia cells through apoptosis and mitotic catastrophe</atitle><jtitle>Cancer letters</jtitle><addtitle>Cancer Lett</addtitle><date>2010-11-28</date><risdate>2010</risdate><volume>297</volume><issue>2</issue><spage>171</spage><epage>181</epage><pages>171-181</pages><issn>0304-3835</issn><eissn>1872-7980</eissn><abstract>Abstract Aurora-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.</abstract><cop>Ireland</cop><pub>Elsevier Ireland Ltd</pub><pmid>20547440</pmid><doi>10.1016/j.canlet.2010.05.009</doi><tpages>11</tpages></addata></record> |
| fulltext | fulltext |
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| ispartof | Cancer letters, 2010-11, Vol.297 (2), p.171-181 |
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| subjects | Acute leukemia Apoptosis Apoptosis - drug effects Ara-C Aurora kinase Aurora Kinases Caspases - metabolism Cell cycle Cell Cycle - drug effects Cell Death - drug effects Cell Line, Tumor Cell Survival Chemotherapy Cytarabine - pharmacology Hematology, Oncology and Palliative Medicine HL-60 Cells Humans Kinases Leukemia Leukemia, Myeloid, Acute - drug therapy Leukemia, Myeloid, Acute - enzymology Leukemia, Myeloid, Acute - pathology Leukemia, Myeloid, Acute - therapy Membrane Potential, Mitochondrial - drug effects Mitochondria - drug effects Mitochondria - genetics Mitochondria - metabolism Mitosis - drug effects Mitotic catastrophe p38 Mitogen-Activated Protein Kinases - metabolism Protein-Serine-Threonine Kinases - antagonists & inhibitors Protein-Serine-Threonine Kinases - genetics RNA, Small Interfering - administration & dosage RNA, Small Interfering - genetics Transfection |
| title | Aurora-A kinase inhibition enhances the cytosine arabinoside-induced cell death in leukemia cells through apoptosis and mitotic catastrophe |
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