Apoptotic mechanisms in T47D and MCF-7 human breast cancer cells
To investigate the mechanisms underlying apoptosis in breast cancer cells, staurosporine was used as an apoptotic stimulus in the human breast cancer cell lines MCF-7 and T47D. Staurosporine induced dose and time dependent increases in DNA fragmentation which was abrogated by z-VAD-fmk. MCF-7 cells...
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| Veröffentlicht in: | British journal of cancer 2002-10, Vol.87 (8), p.909-917 |
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| creator | Mooney, L M Al-Sakkaf, K A Brown, B L Dobson, P R M |
| description | To investigate the mechanisms underlying apoptosis in breast cancer cells, staurosporine was used as an apoptotic stimulus in the human breast cancer cell lines MCF-7 and T47D. Staurosporine induced dose and time dependent increases in DNA fragmentation which was abrogated by z-VAD-fmk. MCF-7 cells did not express caspase-3, suggesting that DNA fragmentation occurred in the absence of caspase-3 and that other caspases may be involved. Staurosporine induced DEVDase activity in T47D cells suggesting the involvement of caspase-3 and/or caspase-7, yet there was no DEVDase activity in MCF-7 cells, probably ruling out the involvement caspase-7. However, staurosporine induced the cleavage of pro-caspase-6 in MCF-7 cells, but not in T47D cells. Caspase dependent PARP cleavage was detected in MCF-7 cells at 3 h, whereas only partial PARP cleavage was detected in T47D cells and then only after 24 h. Moreover, staurosporine led to cytochrome
c
release at 2 h in MCF-7 cells and 6 h in T47D cells. In addition, a time dependent and caspase-independent reduction of the mitochondrial transmembrane potential was observed; which appeared to occur after the release of cytochrome
c
. Translocation of Bax from the cytosol to mitochondria was observed in both cell types, and this preceded cytochrome
c
release in both T47D and MCF-7 cells. Apoptotic events in both cell types differ temporally, involving activation of different caspases and mitochondrial changes. |
| doi_str_mv | 10.1038/sj.bjc.6600541 |
| format | Article |
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c
release at 2 h in MCF-7 cells and 6 h in T47D cells. In addition, a time dependent and caspase-independent reduction of the mitochondrial transmembrane potential was observed; which appeared to occur after the release of cytochrome
c
. Translocation of Bax from the cytosol to mitochondria was observed in both cell types, and this preceded cytochrome
c
release in both T47D and MCF-7 cells. Apoptotic events in both cell types differ temporally, involving activation of different caspases and mitochondrial changes.</description><identifier>ISSN: 0007-0920</identifier><identifier>EISSN: 1532-1827</identifier><identifier>DOI: 10.1038/sj.bjc.6600541</identifier><identifier>PMID: 12373608</identifier><identifier>CODEN: BJCAAI</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>Amino Acid Chloromethyl Ketones ; Apoptosis - drug effects ; bcl-2 Homologous Antagonist-Killer Protein ; bcl-2-Associated X Protein ; bcl-X Protein ; Biological and medical sciences ; Biomedical and Life Sciences ; Biomedicine ; Breast cancer ; Breast Neoplasms - metabolism ; Breast Neoplasms - pathology ; Cancer Research ; Caspase Inhibitors ; Caspases - metabolism ; Cytochrome c Group - metabolism ; Drug Resistance ; Enzyme Activation ; Enzyme Inhibitors - pharmacology ; Epidemiology ; Experimental Therapeutics ; Gynecology. Andrology. Obstetrics ; Humans ; In Situ Nick-End Labeling ; Mammary gland diseases ; Medical sciences ; Membrane Potentials - drug effects ; Membrane Proteins - metabolism ; Mitochondria - drug effects ; Mitochondria - physiology ; Molecular Medicine ; Oncology ; Poly(ADP-ribose) Polymerases - metabolism ; Protein Transport ; Proto-Oncogene Proteins - metabolism ; Proto-Oncogene Proteins c-bcl-2 - metabolism ; Staurosporine - pharmacology ; Tumor Cells, Cultured - drug effects ; Tumor Cells, Cultured - metabolism ; Tumor Suppressor Protein p53 - metabolism ; Tumors</subject><ispartof>British journal of cancer, 2002-10, Vol.87 (8), p.909-917</ispartof><rights>The Author(s) 2002</rights><rights>2003 INIST-CNRS</rights><rights>Copyright 2002 Cancer Research UK</rights><rights>Copyright Nature Publishing Group Oct 7, 2002</rights><rights>Copyright © 2002 Cancer Research UK 2002 Cancer Research UK</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c549t-4b1c4959980595b4a36904455317f067e9b26d9a66d04a863d84dddb1457fd853</citedby><cites>FETCH-LOGICAL-c549t-4b1c4959980595b4a36904455317f067e9b26d9a66d04a863d84dddb1457fd853</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2376174/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2376174/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,41464,42533,51294,53766,53768</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=14353765$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12373608$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Mooney, L M</creatorcontrib><creatorcontrib>Al-Sakkaf, K A</creatorcontrib><creatorcontrib>Brown, B L</creatorcontrib><creatorcontrib>Dobson, P R M</creatorcontrib><title>Apoptotic mechanisms in T47D and MCF-7 human breast cancer cells</title><title>British journal of cancer</title><addtitle>Br J Cancer</addtitle><addtitle>Br J Cancer</addtitle><description>To investigate the mechanisms underlying apoptosis in breast cancer cells, staurosporine was used as an apoptotic stimulus in the human breast cancer cell lines MCF-7 and T47D. Staurosporine induced dose and time dependent increases in DNA fragmentation which was abrogated by z-VAD-fmk. MCF-7 cells did not express caspase-3, suggesting that DNA fragmentation occurred in the absence of caspase-3 and that other caspases may be involved. Staurosporine induced DEVDase activity in T47D cells suggesting the involvement of caspase-3 and/or caspase-7, yet there was no DEVDase activity in MCF-7 cells, probably ruling out the involvement caspase-7. However, staurosporine induced the cleavage of pro-caspase-6 in MCF-7 cells, but not in T47D cells. Caspase dependent PARP cleavage was detected in MCF-7 cells at 3 h, whereas only partial PARP cleavage was detected in T47D cells and then only after 24 h. Moreover, staurosporine led to cytochrome
c
release at 2 h in MCF-7 cells and 6 h in T47D cells. In addition, a time dependent and caspase-independent reduction of the mitochondrial transmembrane potential was observed; which appeared to occur after the release of cytochrome
c
. Translocation of Bax from the cytosol to mitochondria was observed in both cell types, and this preceded cytochrome
c
release in both T47D and MCF-7 cells. Apoptotic events in both cell types differ temporally, involving activation of different caspases and mitochondrial changes.</description><subject>Amino Acid Chloromethyl Ketones</subject><subject>Apoptosis - drug effects</subject><subject>bcl-2 Homologous Antagonist-Killer Protein</subject><subject>bcl-2-Associated X Protein</subject><subject>bcl-X Protein</subject><subject>Biological and medical sciences</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Breast cancer</subject><subject>Breast Neoplasms - metabolism</subject><subject>Breast Neoplasms - pathology</subject><subject>Cancer Research</subject><subject>Caspase Inhibitors</subject><subject>Caspases - metabolism</subject><subject>Cytochrome c Group - metabolism</subject><subject>Drug Resistance</subject><subject>Enzyme Activation</subject><subject>Enzyme Inhibitors - pharmacology</subject><subject>Epidemiology</subject><subject>Experimental Therapeutics</subject><subject>Gynecology. Andrology. Obstetrics</subject><subject>Humans</subject><subject>In Situ Nick-End Labeling</subject><subject>Mammary gland diseases</subject><subject>Medical sciences</subject><subject>Membrane Potentials - drug effects</subject><subject>Membrane Proteins - metabolism</subject><subject>Mitochondria - drug effects</subject><subject>Mitochondria - physiology</subject><subject>Molecular Medicine</subject><subject>Oncology</subject><subject>Poly(ADP-ribose) Polymerases - metabolism</subject><subject>Protein Transport</subject><subject>Proto-Oncogene Proteins - metabolism</subject><subject>Proto-Oncogene Proteins c-bcl-2 - metabolism</subject><subject>Staurosporine - pharmacology</subject><subject>Tumor Cells, Cultured - drug effects</subject><subject>Tumor Cells, Cultured - metabolism</subject><subject>Tumor Suppressor Protein p53 - metabolism</subject><subject>Tumors</subject><issn>0007-0920</issn><issn>1532-1827</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp1kM1P4zAQxS3ECrosV47IQuKYYsffFwQqW3YlVnspZ8uxHZoocYqdIvHfY9SIwoHTaDS_efPmAXCG0RwjIq9SO69aO-ccIUbxAZhhRsoCy1IcghlCSBRIlegY_Eypza1CUhyBY1wSQTiSM3Bzuxk24zA2Fvberk1oUp9gE-CKijtogoP_FstCwPW2NwFW0Zs0QmuC9RFa33XpF_hRmy7506megMfl79XiT_Hw__7v4vahsIyqsaAVtlQxpSRiilXUEK4QpYwRLGrEhVdVyZ0ynDtEjeTESeqcqzBlonaSkRNwvdPdbKveO-vDGE2nN7HpTXzVg2n010lo1vppeNH5VY4FzQIXk0Acnrc-jbodtjFkz7osleJCSpmh-Q6ycUgp-vrjAEb6PXCdWp0D11PgeeH8s609PiWcgcsJMMmaro45uybtOUpYNvj-39WOS3kUnnzc2_vm9BuEHJdE</recordid><startdate>20021007</startdate><enddate>20021007</enddate><creator>Mooney, L M</creator><creator>Al-Sakkaf, K A</creator><creator>Brown, B L</creator><creator>Dobson, P R M</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</general><scope>C6C</scope><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>3V.</scope><scope>7RV</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB0</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>5PM</scope></search><sort><creationdate>20021007</creationdate><title>Apoptotic mechanisms in T47D and MCF-7 human breast cancer cells</title><author>Mooney, L M ; Al-Sakkaf, K A ; Brown, B L ; Dobson, P R M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c549t-4b1c4959980595b4a36904455317f067e9b26d9a66d04a863d84dddb1457fd853</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Amino Acid Chloromethyl Ketones</topic><topic>Apoptosis - drug effects</topic><topic>bcl-2 Homologous Antagonist-Killer Protein</topic><topic>bcl-2-Associated X Protein</topic><topic>bcl-X Protein</topic><topic>Biological and medical sciences</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Breast cancer</topic><topic>Breast Neoplasms - metabolism</topic><topic>Breast Neoplasms - pathology</topic><topic>Cancer Research</topic><topic>Caspase Inhibitors</topic><topic>Caspases - metabolism</topic><topic>Cytochrome c Group - metabolism</topic><topic>Drug Resistance</topic><topic>Enzyme Activation</topic><topic>Enzyme Inhibitors - pharmacology</topic><topic>Epidemiology</topic><topic>Experimental Therapeutics</topic><topic>Gynecology. Andrology. Obstetrics</topic><topic>Humans</topic><topic>In Situ Nick-End Labeling</topic><topic>Mammary gland diseases</topic><topic>Medical sciences</topic><topic>Membrane Potentials - drug effects</topic><topic>Membrane Proteins - metabolism</topic><topic>Mitochondria - drug effects</topic><topic>Mitochondria - physiology</topic><topic>Molecular Medicine</topic><topic>Oncology</topic><topic>Poly(ADP-ribose) Polymerases - metabolism</topic><topic>Protein Transport</topic><topic>Proto-Oncogene Proteins - metabolism</topic><topic>Proto-Oncogene Proteins c-bcl-2 - metabolism</topic><topic>Staurosporine - pharmacology</topic><topic>Tumor Cells, Cultured - drug effects</topic><topic>Tumor Cells, Cultured - metabolism</topic><topic>Tumor Suppressor Protein p53 - metabolism</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Mooney, L M</creatorcontrib><creatorcontrib>Al-Sakkaf, K A</creatorcontrib><creatorcontrib>Brown, B L</creatorcontrib><creatorcontrib>Dobson, P R M</creatorcontrib><collection>Springer Nature OA Free Journals</collection><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>ProQuest Central (Corporate)</collection><collection>Nursing & Allied Health Database</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health 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>British Nursing Database</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</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>Nursing & Allied Health Database (Alumni Edition)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>Nursing & Allied Health Premium</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>British journal of cancer</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Mooney, L M</au><au>Al-Sakkaf, K A</au><au>Brown, B L</au><au>Dobson, P R M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Apoptotic mechanisms in T47D and MCF-7 human breast cancer cells</atitle><jtitle>British journal of cancer</jtitle><stitle>Br J Cancer</stitle><addtitle>Br J Cancer</addtitle><date>2002-10-07</date><risdate>2002</risdate><volume>87</volume><issue>8</issue><spage>909</spage><epage>917</epage><pages>909-917</pages><issn>0007-0920</issn><eissn>1532-1827</eissn><coden>BJCAAI</coden><abstract>To investigate the mechanisms underlying apoptosis in breast cancer cells, staurosporine was used as an apoptotic stimulus in the human breast cancer cell lines MCF-7 and T47D. Staurosporine induced dose and time dependent increases in DNA fragmentation which was abrogated by z-VAD-fmk. MCF-7 cells did not express caspase-3, suggesting that DNA fragmentation occurred in the absence of caspase-3 and that other caspases may be involved. Staurosporine induced DEVDase activity in T47D cells suggesting the involvement of caspase-3 and/or caspase-7, yet there was no DEVDase activity in MCF-7 cells, probably ruling out the involvement caspase-7. However, staurosporine induced the cleavage of pro-caspase-6 in MCF-7 cells, but not in T47D cells. Caspase dependent PARP cleavage was detected in MCF-7 cells at 3 h, whereas only partial PARP cleavage was detected in T47D cells and then only after 24 h. Moreover, staurosporine led to cytochrome
c
release at 2 h in MCF-7 cells and 6 h in T47D cells. In addition, a time dependent and caspase-independent reduction of the mitochondrial transmembrane potential was observed; which appeared to occur after the release of cytochrome
c
. Translocation of Bax from the cytosol to mitochondria was observed in both cell types, and this preceded cytochrome
c
release in both T47D and MCF-7 cells. Apoptotic events in both cell types differ temporally, involving activation of different caspases and mitochondrial changes.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>12373608</pmid><doi>10.1038/sj.bjc.6600541</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | British journal of cancer, 2002-10, Vol.87 (8), p.909-917 |
| issn | 0007-0920 1532-1827 |
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| subjects | Amino Acid Chloromethyl Ketones Apoptosis - drug effects bcl-2 Homologous Antagonist-Killer Protein bcl-2-Associated X Protein bcl-X Protein Biological and medical sciences Biomedical and Life Sciences Biomedicine Breast cancer Breast Neoplasms - metabolism Breast Neoplasms - pathology Cancer Research Caspase Inhibitors Caspases - metabolism Cytochrome c Group - metabolism Drug Resistance Enzyme Activation Enzyme Inhibitors - pharmacology Epidemiology Experimental Therapeutics Gynecology. Andrology. Obstetrics Humans In Situ Nick-End Labeling Mammary gland diseases Medical sciences Membrane Potentials - drug effects Membrane Proteins - metabolism Mitochondria - drug effects Mitochondria - physiology Molecular Medicine Oncology Poly(ADP-ribose) Polymerases - metabolism Protein Transport Proto-Oncogene Proteins - metabolism Proto-Oncogene Proteins c-bcl-2 - metabolism Staurosporine - pharmacology Tumor Cells, Cultured - drug effects Tumor Cells, Cultured - metabolism Tumor Suppressor Protein p53 - metabolism Tumors |
| title | Apoptotic mechanisms in T47D and MCF-7 human breast cancer cells |
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