Cyclin E overexpression enhances cytokine-mediated apoptosis in MCF7 breast cancer cells
Cyclin E, the regulatory component of the cyclin E/cyclin-dependent kinase (CDK) complex, is required for proliferation and overexpression of this cyclin is associated with many types of human tumors. To elucidate the mechanism by which cyclin E overexpression promotes tumorigenesis, cyclin E was ov...
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| Veröffentlicht in: | Genes and immunity 2003-07, Vol.4 (5), p.336-342 |
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| description | Cyclin E, the regulatory component of the cyclin E/cyclin-dependent kinase (CDK) complex, is required for proliferation and overexpression of this cyclin is associated with many types of human tumors. To elucidate the mechanism by which cyclin E overexpression promotes tumorigenesis, cyclin E was overexpressed in two breast cancer lines: MCF7 and T47D. Cells overexpressing cyclin E display a marked decrease in the expression of Bcl-2, an antiapoptotic protein, and increased levels of the proapoptotic proteins Bad and Bax. The levels of Bcl-X
L
and Mcl-1 remain unchanged. Since the homeostasis of pro- and antiapoptotic proteins was altered, we asked if cyclin E overexpression modifies responses to cytokines. MCF7 cyclin E overexpressing cells have an enhanced sensitivity to Fas, TRAIL, and TNF-α-induced apoptosis. T47D cells overexpressing cyclin E have a significant increase in TNF-α and TRAIL-induced apoptosis. In conclusion, our results provide a link between expression of cyclin E, deregulation of Bcl-2, and an altered response to cytokine-mediated apoptosis. |
| doi_str_mv | 10.1038/sj.gene.6363973 |
| format | Article |
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L
and Mcl-1 remain unchanged. Since the homeostasis of pro- and antiapoptotic proteins was altered, we asked if cyclin E overexpression modifies responses to cytokines. MCF7 cyclin E overexpressing cells have an enhanced sensitivity to Fas, TRAIL, and TNF-α-induced apoptosis. T47D cells overexpressing cyclin E have a significant increase in TNF-α and TRAIL-induced apoptosis. In conclusion, our results provide a link between expression of cyclin E, deregulation of Bcl-2, and an altered response to cytokine-mediated apoptosis.</description><identifier>ISSN: 1466-4879</identifier><identifier>EISSN: 1476-5470</identifier><identifier>DOI: 10.1038/sj.gene.6363973</identifier><identifier>PMID: 12847548</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>Apoptosis ; Apoptosis - genetics ; Apoptosis - physiology ; Apoptosis Regulatory Proteins ; Bax protein ; Bcl-2 protein ; Bcl-x protein ; Biological and medical sciences ; Biomedical and Life Sciences ; Biomedicine ; Blotting, Western ; Breast cancer ; Breast Neoplasms - genetics ; Breast Neoplasms - metabolism ; Cancer cells ; Cancer Research ; Cell Line, Tumor ; Cyclin E ; Cyclin E - genetics ; Cyclin E - metabolism ; Cyclin-dependent kinase ; Cyclin-dependent kinases ; Cytokines ; Cytokines - metabolism ; Death Domain Receptor Signaling Adaptor Proteins ; full-paper ; Fundamental and applied biological sciences. Psychology ; Gene Expression ; Health aspects ; Homeostasis ; Human Genetics ; Humans ; Immunology ; Kinases ; Mcl-1 protein ; Membrane Glycoproteins - metabolism ; Microbiology ; Physiological aspects ; Receptors, Tumor Necrosis Factor - metabolism ; Risk factors ; TNF-Related Apoptosis-Inducing Ligand ; Tumor Necrosis Factor-alpha - metabolism ; Tumor necrosis factor-α ; Tumorigenesis</subject><ispartof>Genes and immunity, 2003-07, Vol.4 (5), p.336-342</ispartof><rights>Springer Nature Limited 2003</rights><rights>2003 INIST-CNRS</rights><rights>COPYRIGHT 2003 Nature Publishing Group</rights><rights>Copyright Nature Publishing Group Jul 2003</rights><rights>Nature Publishing Group 2003.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c551t-bbd82469c47e2e1d7130a0aed36bcd6d986b0d2fd819dedb412ca80aee531a193</citedby><cites>FETCH-LOGICAL-c551t-bbd82469c47e2e1d7130a0aed36bcd6d986b0d2fd819dedb412ca80aee531a193</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1038/sj.gene.6363973$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/sj.gene.6363973$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=14995087$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12847548$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Dhillon, N K</creatorcontrib><creatorcontrib>Mudryj, M</creatorcontrib><title>Cyclin E overexpression enhances cytokine-mediated apoptosis in MCF7 breast cancer cells</title><title>Genes and immunity</title><addtitle>Genes Immun</addtitle><addtitle>Genes Immun</addtitle><description>Cyclin E, the regulatory component of the cyclin E/cyclin-dependent kinase (CDK) complex, is required for proliferation and overexpression of this cyclin is associated with many types of human tumors. To elucidate the mechanism by which cyclin E overexpression promotes tumorigenesis, cyclin E was overexpressed in two breast cancer lines: MCF7 and T47D. Cells overexpressing cyclin E display a marked decrease in the expression of Bcl-2, an antiapoptotic protein, and increased levels of the proapoptotic proteins Bad and Bax. The levels of Bcl-X
L
and Mcl-1 remain unchanged. Since the homeostasis of pro- and antiapoptotic proteins was altered, we asked if cyclin E overexpression modifies responses to cytokines. MCF7 cyclin E overexpressing cells have an enhanced sensitivity to Fas, TRAIL, and TNF-α-induced apoptosis. T47D cells overexpressing cyclin E have a significant increase in TNF-α and TRAIL-induced apoptosis. In conclusion, our results provide a link between expression of cyclin E, deregulation of Bcl-2, and an altered response to cytokine-mediated apoptosis.</description><subject>Apoptosis</subject><subject>Apoptosis - genetics</subject><subject>Apoptosis - physiology</subject><subject>Apoptosis Regulatory Proteins</subject><subject>Bax protein</subject><subject>Bcl-2 protein</subject><subject>Bcl-x protein</subject><subject>Biological and medical sciences</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Blotting, Western</subject><subject>Breast cancer</subject><subject>Breast Neoplasms - genetics</subject><subject>Breast Neoplasms - metabolism</subject><subject>Cancer cells</subject><subject>Cancer Research</subject><subject>Cell Line, Tumor</subject><subject>Cyclin E</subject><subject>Cyclin E - genetics</subject><subject>Cyclin E - metabolism</subject><subject>Cyclin-dependent kinase</subject><subject>Cyclin-dependent kinases</subject><subject>Cytokines</subject><subject>Cytokines - metabolism</subject><subject>Death Domain Receptor Signaling Adaptor Proteins</subject><subject>full-paper</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Gene Expression</subject><subject>Health aspects</subject><subject>Homeostasis</subject><subject>Human Genetics</subject><subject>Humans</subject><subject>Immunology</subject><subject>Kinases</subject><subject>Mcl-1 protein</subject><subject>Membrane Glycoproteins - metabolism</subject><subject>Microbiology</subject><subject>Physiological aspects</subject><subject>Receptors, Tumor Necrosis Factor - metabolism</subject><subject>Risk factors</subject><subject>TNF-Related Apoptosis-Inducing Ligand</subject><subject>Tumor Necrosis Factor-alpha - metabolism</subject><subject>Tumor necrosis factor-α</subject><subject>Tumorigenesis</subject><issn>1466-4879</issn><issn>1476-5470</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNqFkt1rFDEUxQdRbK0--yaDouDDbJNJJh-PZWlroSL4Ab6FTHJnzTqb2ebOSve_b4ZdWFYskoeE5HfOzU1OUbymZEYJU-e4nC0gwkwwwbRkT4pTyqWoGi7J02ktRMWV1CfFC8QlIVRQoZ8XJ7RWXDZcnRY_51vXh1helsMfSHC_ToAYhlhC_GWjAyzddhx-hwjVCnywI_jSrof1OGDAMgs_z69k2SawOJZuUqTSQd_jy-JZZ3uEV_v5rPhxdfl9_qm6_XJ9M7-4rVzT0LFqW69qLrTjEmqgXlJGLLHgmWidF14r0RJfd15R7cG3nNbOqgxAw6ilmp0VH3a-6zTcbQBHswo43cBGGDZoJOON4jX5L0iVIpJwlsF3f4HLYZNibsLUglNZK9E0mXr7KJWtNFOaHKwWtgcTYjeMybqprrmgqtasYWqymv2DysPDKrghQhfy_pHg45EgMyPcjwu7QTQ3374es-c71qUBMUFn1imsbNoaSsyUIYNLM2XI7DOUFW_2nW3a_OcHfh-aDLzfAxad7buUvz3ggeNaN0TJzJEdh_koLiAdnuix2g8BLd1d</recordid><startdate>20030701</startdate><enddate>20030701</enddate><creator>Dhillon, N K</creator><creator>Mudryj, M</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</general><scope>IQODW</scope><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>ISR</scope><scope>3V.</scope><scope>7T5</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20030701</creationdate><title>Cyclin E overexpression enhances cytokine-mediated apoptosis in MCF7 breast cancer cells</title><author>Dhillon, N K ; Mudryj, M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c551t-bbd82469c47e2e1d7130a0aed36bcd6d986b0d2fd819dedb412ca80aee531a193</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Apoptosis</topic><topic>Apoptosis - genetics</topic><topic>Apoptosis - physiology</topic><topic>Apoptosis Regulatory Proteins</topic><topic>Bax protein</topic><topic>Bcl-2 protein</topic><topic>Bcl-x protein</topic><topic>Biological and medical sciences</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Blotting, Western</topic><topic>Breast cancer</topic><topic>Breast Neoplasms - genetics</topic><topic>Breast Neoplasms - metabolism</topic><topic>Cancer cells</topic><topic>Cancer Research</topic><topic>Cell Line, Tumor</topic><topic>Cyclin E</topic><topic>Cyclin E - genetics</topic><topic>Cyclin E - metabolism</topic><topic>Cyclin-dependent kinase</topic><topic>Cyclin-dependent kinases</topic><topic>Cytokines</topic><topic>Cytokines - metabolism</topic><topic>Death Domain Receptor Signaling Adaptor Proteins</topic><topic>full-paper</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Gene Expression</topic><topic>Health aspects</topic><topic>Homeostasis</topic><topic>Human Genetics</topic><topic>Humans</topic><topic>Immunology</topic><topic>Kinases</topic><topic>Mcl-1 protein</topic><topic>Membrane Glycoproteins - metabolism</topic><topic>Microbiology</topic><topic>Physiological aspects</topic><topic>Receptors, Tumor Necrosis Factor - metabolism</topic><topic>Risk factors</topic><topic>TNF-Related Apoptosis-Inducing Ligand</topic><topic>Tumor Necrosis Factor-alpha - metabolism</topic><topic>Tumor necrosis factor-α</topic><topic>Tumorigenesis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Dhillon, N K</creatorcontrib><creatorcontrib>Mudryj, M</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale In Context: Science</collection><collection>ProQuest Central (Corporate)</collection><collection>Immunology Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection (ProQuest)</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Genes and immunity</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Dhillon, N K</au><au>Mudryj, M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cyclin E overexpression enhances cytokine-mediated apoptosis in MCF7 breast cancer cells</atitle><jtitle>Genes and immunity</jtitle><stitle>Genes Immun</stitle><addtitle>Genes Immun</addtitle><date>2003-07-01</date><risdate>2003</risdate><volume>4</volume><issue>5</issue><spage>336</spage><epage>342</epage><pages>336-342</pages><issn>1466-4879</issn><eissn>1476-5470</eissn><abstract>Cyclin E, the regulatory component of the cyclin E/cyclin-dependent kinase (CDK) complex, is required for proliferation and overexpression of this cyclin is associated with many types of human tumors. To elucidate the mechanism by which cyclin E overexpression promotes tumorigenesis, cyclin E was overexpressed in two breast cancer lines: MCF7 and T47D. Cells overexpressing cyclin E display a marked decrease in the expression of Bcl-2, an antiapoptotic protein, and increased levels of the proapoptotic proteins Bad and Bax. The levels of Bcl-X
L
and Mcl-1 remain unchanged. Since the homeostasis of pro- and antiapoptotic proteins was altered, we asked if cyclin E overexpression modifies responses to cytokines. MCF7 cyclin E overexpressing cells have an enhanced sensitivity to Fas, TRAIL, and TNF-α-induced apoptosis. T47D cells overexpressing cyclin E have a significant increase in TNF-α and TRAIL-induced apoptosis. In conclusion, our results provide a link between expression of cyclin E, deregulation of Bcl-2, and an altered response to cytokine-mediated apoptosis.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>12847548</pmid><doi>10.1038/sj.gene.6363973</doi><tpages>7</tpages></addata></record> |
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| subjects | Apoptosis Apoptosis - genetics Apoptosis - physiology Apoptosis Regulatory Proteins Bax protein Bcl-2 protein Bcl-x protein Biological and medical sciences Biomedical and Life Sciences Biomedicine Blotting, Western Breast cancer Breast Neoplasms - genetics Breast Neoplasms - metabolism Cancer cells Cancer Research Cell Line, Tumor Cyclin E Cyclin E - genetics Cyclin E - metabolism Cyclin-dependent kinase Cyclin-dependent kinases Cytokines Cytokines - metabolism Death Domain Receptor Signaling Adaptor Proteins full-paper Fundamental and applied biological sciences. Psychology Gene Expression Health aspects Homeostasis Human Genetics Humans Immunology Kinases Mcl-1 protein Membrane Glycoproteins - metabolism Microbiology Physiological aspects Receptors, Tumor Necrosis Factor - metabolism Risk factors TNF-Related Apoptosis-Inducing Ligand Tumor Necrosis Factor-alpha - metabolism Tumor necrosis factor-α Tumorigenesis |
| title | Cyclin E overexpression enhances cytokine-mediated apoptosis in MCF7 breast cancer cells |
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