Resistance of mitochondrial DNA-deficient cells to TRAIL: Role of Bax in TRAIL-induced apoptosis
Mitochondrion is one of the master players in both apoptosis and necrosis. We studied the role of mitochondrial function in TRAIL-induced apoptosis. TRAIL killed SK-Hep1 cells with characteristic features of apoptosis such as DNA fragmentation, sub-G1 ploidy peak and cytochrome c translocation. In c...
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| Veröffentlicht in: | Oncogene 2002-05, Vol.21 (20), p.3139-3148 |
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| creator | KIM, Ja-Young KIM, Yun-Hee INIK CHANG SUNSHIN KIM YOUNGMI KIM PAK OH, Byung-Ha YAGITA, Hideo YONG KEUN JUNG YOUNG JOON OH LEE, Myung-Shik |
| description | Mitochondrion is one of the master players in both apoptosis and necrosis. We studied the role of mitochondrial function in TRAIL-induced apoptosis. TRAIL killed SK-Hep1 cells with characteristic features of apoptosis such as DNA fragmentation, sub-G1 ploidy peak and cytochrome c translocation. In contrast, mitochondrial DNA-deficient SK-Hep1 rho(0) cells were resistant to TRAIL. Dissipation of mitochondrial potential or cytochrome c translocation did not occur in rho(0) cells after TRAIL treatment. TRAIL induced translocation of Bax subsequent to the cleavage of Bid in parental cells. However, Bax translocation was absent in rho(0) cells, accounting for the failure of cytochrome c release in rho(0) cells. Forced expression of Bax induced caspase-3 activity in rho(0) cells. Incubation of rho(0) cells with ADP+Pi to increase intracellular ATP restored sensitivity to TRAIL. Despite different sensitivity to TRAIL, parental cells and rho(0) cells did not show significant difference in susceptibility to agonistic anti-Fas antibody, TNF-alpha or staurosporine. Our results indicate that TRAIL-induced apoptosis is dependent on intact mitochondrial function and susceptibility of mitochondrial DNA-deficient cells to apoptosis depends on the type of apoptotic stimuli. Tumor cells with mitochondrial mutations or dysfunction might have the ability to evade tumor surveillance imposed by TRAIL in vivo. |
| doi_str_mv | 10.1038/sj.onc.1205406 |
| format | Article |
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We studied the role of mitochondrial function in TRAIL-induced apoptosis. TRAIL killed SK-Hep1 cells with characteristic features of apoptosis such as DNA fragmentation, sub-G1 ploidy peak and cytochrome c translocation. In contrast, mitochondrial DNA-deficient SK-Hep1 rho(0) cells were resistant to TRAIL. Dissipation of mitochondrial potential or cytochrome c translocation did not occur in rho(0) cells after TRAIL treatment. TRAIL induced translocation of Bax subsequent to the cleavage of Bid in parental cells. However, Bax translocation was absent in rho(0) cells, accounting for the failure of cytochrome c release in rho(0) cells. Forced expression of Bax induced caspase-3 activity in rho(0) cells. Incubation of rho(0) cells with ADP+Pi to increase intracellular ATP restored sensitivity to TRAIL. Despite different sensitivity to TRAIL, parental cells and rho(0) cells did not show significant difference in susceptibility to agonistic anti-Fas antibody, TNF-alpha or staurosporine. Our results indicate that TRAIL-induced apoptosis is dependent on intact mitochondrial function and susceptibility of mitochondrial DNA-deficient cells to apoptosis depends on the type of apoptotic stimuli. Tumor cells with mitochondrial mutations or dysfunction might have the ability to evade tumor surveillance imposed by TRAIL in vivo.</description><identifier>ISSN: 0950-9232</identifier><identifier>EISSN: 1476-5594</identifier><identifier>DOI: 10.1038/sj.onc.1205406</identifier><identifier>PMID: 12082629</identifier><identifier>CODEN: ONCNES</identifier><language>eng</language><publisher>Basingstoke: Nature Publishing</publisher><subject>Adenosine Triphosphate - physiology ; Ageing, cell death ; Apoptosis ; Apoptosis - drug effects ; Apoptosis - physiology ; Apoptosis Regulatory Proteins ; bcl-2-Associated X Protein ; BH3 Interacting Domain Death Agonist Protein ; Biological and medical sciences ; Cancer ; Carcinoma, Hepatocellular - pathology ; Carrier Proteins - metabolism ; Caspase 3 ; Caspase 8 ; Caspase 9 ; Caspases - biosynthesis ; Caspases - metabolism ; Cell death ; Cell physiology ; Cysteine Proteinase Inhibitors - pharmacology ; Cytochrome ; Cytochrome c ; Cytochrome c Group - metabolism ; DNA fragmentation ; DNA, Mitochondrial - drug effects ; DNA, Mitochondrial - physiology ; Enzyme Induction ; Ethidium - pharmacology ; Fundamental and applied biological sciences. Psychology ; Genetic aspects ; Health aspects ; Humans ; Intracellular Membranes - ultrastructure ; Life sciences ; Liver Neoplasms - pathology ; Membrane Glycoproteins - antagonists & inhibitors ; Membrane Glycoproteins - pharmacology ; Membrane Glycoproteins - physiology ; Membrane Potentials ; Mitochondria ; Mitochondria - physiology ; Mitochondria - ultrastructure ; Mitochondrial DNA ; Molecular and cellular biology ; Phosphorylation ; Physiological aspects ; Ploidy ; Protein Transport ; Proto-Oncogene Proteins - physiology ; Proto-Oncogene Proteins c-bcl-2 ; Signal transduction ; Staurosporine ; TNF-Related Apoptosis-Inducing Ligand ; Tumor cells ; Tumor Cells, Cultured - drug effects ; Tumor Cells, Cultured - metabolism ; Tumor necrosis factor ; Tumor Necrosis Factor-alpha - antagonists & inhibitors ; Tumor Necrosis Factor-alpha - pharmacology ; Tumor Necrosis Factor-alpha - physiology ; Tumor necrosis factor-α</subject><ispartof>Oncogene, 2002-05, Vol.21 (20), p.3139-3148</ispartof><rights>2002 INIST-CNRS</rights><rights>COPYRIGHT 2002 Nature Publishing Group</rights><rights>Copyright Nature Publishing Group May 9, 2002</rights><rights>Macmillan Publishers Limited 2002.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c511t-6c2fd64d14b5962428cbe835e2f69daf1612cf3fac3104c0b866e395cee340903</citedby><cites>FETCH-LOGICAL-c511t-6c2fd64d14b5962428cbe835e2f69daf1612cf3fac3104c0b866e395cee340903</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,781,785,27926,27927</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=13767677$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12082629$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>KIM, Ja-Young</creatorcontrib><creatorcontrib>KIM, Yun-Hee</creatorcontrib><creatorcontrib>INIK CHANG</creatorcontrib><creatorcontrib>SUNSHIN KIM</creatorcontrib><creatorcontrib>YOUNGMI KIM PAK</creatorcontrib><creatorcontrib>OH, Byung-Ha</creatorcontrib><creatorcontrib>YAGITA, Hideo</creatorcontrib><creatorcontrib>YONG KEUN JUNG</creatorcontrib><creatorcontrib>YOUNG JOON OH</creatorcontrib><creatorcontrib>LEE, Myung-Shik</creatorcontrib><title>Resistance of mitochondrial DNA-deficient cells to TRAIL: Role of Bax in TRAIL-induced apoptosis</title><title>Oncogene</title><addtitle>Oncogene</addtitle><description>Mitochondrion is one of the master players in both apoptosis and necrosis. We studied the role of mitochondrial function in TRAIL-induced apoptosis. TRAIL killed SK-Hep1 cells with characteristic features of apoptosis such as DNA fragmentation, sub-G1 ploidy peak and cytochrome c translocation. In contrast, mitochondrial DNA-deficient SK-Hep1 rho(0) cells were resistant to TRAIL. Dissipation of mitochondrial potential or cytochrome c translocation did not occur in rho(0) cells after TRAIL treatment. TRAIL induced translocation of Bax subsequent to the cleavage of Bid in parental cells. However, Bax translocation was absent in rho(0) cells, accounting for the failure of cytochrome c release in rho(0) cells. Forced expression of Bax induced caspase-3 activity in rho(0) cells. Incubation of rho(0) cells with ADP+Pi to increase intracellular ATP restored sensitivity to TRAIL. Despite different sensitivity to TRAIL, parental cells and rho(0) cells did not show significant difference in susceptibility to agonistic anti-Fas antibody, TNF-alpha or staurosporine. Our results indicate that TRAIL-induced apoptosis is dependent on intact mitochondrial function and susceptibility of mitochondrial DNA-deficient cells to apoptosis depends on the type of apoptotic stimuli. Tumor cells with mitochondrial mutations or dysfunction might have the ability to evade tumor surveillance imposed by TRAIL in vivo.</description><subject>Adenosine Triphosphate - physiology</subject><subject>Ageing, cell death</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Apoptosis - physiology</subject><subject>Apoptosis Regulatory Proteins</subject><subject>bcl-2-Associated X Protein</subject><subject>BH3 Interacting Domain Death Agonist Protein</subject><subject>Biological and medical sciences</subject><subject>Cancer</subject><subject>Carcinoma, Hepatocellular - pathology</subject><subject>Carrier Proteins - metabolism</subject><subject>Caspase 3</subject><subject>Caspase 8</subject><subject>Caspase 9</subject><subject>Caspases - biosynthesis</subject><subject>Caspases - metabolism</subject><subject>Cell death</subject><subject>Cell physiology</subject><subject>Cysteine Proteinase Inhibitors - pharmacology</subject><subject>Cytochrome</subject><subject>Cytochrome c</subject><subject>Cytochrome c Group - metabolism</subject><subject>DNA fragmentation</subject><subject>DNA, Mitochondrial - drug effects</subject><subject>DNA, Mitochondrial - physiology</subject><subject>Enzyme Induction</subject><subject>Ethidium - pharmacology</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Genetic aspects</subject><subject>Health aspects</subject><subject>Humans</subject><subject>Intracellular Membranes - ultrastructure</subject><subject>Life sciences</subject><subject>Liver Neoplasms - pathology</subject><subject>Membrane Glycoproteins - antagonists & inhibitors</subject><subject>Membrane Glycoproteins - pharmacology</subject><subject>Membrane Glycoproteins - physiology</subject><subject>Membrane Potentials</subject><subject>Mitochondria</subject><subject>Mitochondria - physiology</subject><subject>Mitochondria - ultrastructure</subject><subject>Mitochondrial DNA</subject><subject>Molecular and cellular biology</subject><subject>Phosphorylation</subject><subject>Physiological aspects</subject><subject>Ploidy</subject><subject>Protein Transport</subject><subject>Proto-Oncogene Proteins - physiology</subject><subject>Proto-Oncogene Proteins c-bcl-2</subject><subject>Signal transduction</subject><subject>Staurosporine</subject><subject>TNF-Related Apoptosis-Inducing Ligand</subject><subject>Tumor cells</subject><subject>Tumor Cells, Cultured - drug effects</subject><subject>Tumor Cells, Cultured - metabolism</subject><subject>Tumor necrosis factor</subject><subject>Tumor Necrosis Factor-alpha - antagonists & inhibitors</subject><subject>Tumor Necrosis Factor-alpha - pharmacology</subject><subject>Tumor Necrosis Factor-alpha - physiology</subject><subject>Tumor necrosis factor-α</subject><issn>0950-9232</issn><issn>1476-5594</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNp1kUuLFDEUhYMoTju6dSmFortq866Ku3Z8DTQKzbiO6eRG01QlbVIF-u9NOwUNMnIXgct3Tg73IPSU4DXBrH9dDusU7ZpQLDiW99CK8E62Qih-H62wErhVlNEL9KiUA8a4U5g-RBcV76mkaoW-7aCEMplooUm-GcOU7I8UXQ5maN593rQOfLAB4tRYGIbSTKm52W2ut2-aXRr-at6aX02It9s2RDdbcI05puOUqvVj9MCbocCT5b1EXz-8v7n61G6_fLy-2mxbKwiZWmmpd5I7wvdCScppb_fQMwHUS-WMJ5JQ65k3lhHMLd73UgJTwgIwjhVml-jVre8xp58zlEmPoZwimwhpLrojvSCUdhV88Q94SHOONZumkhNGOCa8Us__S1UTQit4tvpuBtAh-jRlY0__6k0tRKgOK1ap9R1UHQdjsCnWA9f9XQKbUykZvD7mMJr8WxOsT63rctC1db20XgXPlrDzfgR3xpeaK_ByAUyxZvC59h3KmWOdrNOxP9tfsSI</recordid><startdate>20020509</startdate><enddate>20020509</enddate><creator>KIM, Ja-Young</creator><creator>KIM, Yun-Hee</creator><creator>INIK CHANG</creator><creator>SUNSHIN KIM</creator><creator>YOUNGMI KIM PAK</creator><creator>OH, Byung-Ha</creator><creator>YAGITA, Hideo</creator><creator>YONG KEUN JUNG</creator><creator>YOUNG JOON OH</creator><creator>LEE, Myung-Shik</creator><general>Nature Publishing</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>3V.</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</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>8G5</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>GUQSH</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>M7P</scope><scope>MBDVC</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20020509</creationdate><title>Resistance of mitochondrial DNA-deficient cells to TRAIL: Role of Bax in TRAIL-induced apoptosis</title><author>KIM, Ja-Young ; KIM, Yun-Hee ; INIK CHANG ; SUNSHIN KIM ; YOUNGMI KIM PAK ; OH, Byung-Ha ; YAGITA, Hideo ; YONG KEUN JUNG ; YOUNG JOON OH ; LEE, Myung-Shik</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c511t-6c2fd64d14b5962428cbe835e2f69daf1612cf3fac3104c0b866e395cee340903</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Adenosine Triphosphate - physiology</topic><topic>Ageing, cell death</topic><topic>Apoptosis</topic><topic>Apoptosis - drug effects</topic><topic>Apoptosis - physiology</topic><topic>Apoptosis Regulatory Proteins</topic><topic>bcl-2-Associated X Protein</topic><topic>BH3 Interacting Domain Death Agonist Protein</topic><topic>Biological and medical sciences</topic><topic>Cancer</topic><topic>Carcinoma, Hepatocellular - pathology</topic><topic>Carrier Proteins - metabolism</topic><topic>Caspase 3</topic><topic>Caspase 8</topic><topic>Caspase 9</topic><topic>Caspases - biosynthesis</topic><topic>Caspases - metabolism</topic><topic>Cell death</topic><topic>Cell physiology</topic><topic>Cysteine Proteinase Inhibitors - pharmacology</topic><topic>Cytochrome</topic><topic>Cytochrome c</topic><topic>Cytochrome c Group - metabolism</topic><topic>DNA fragmentation</topic><topic>DNA, Mitochondrial - drug effects</topic><topic>DNA, Mitochondrial - physiology</topic><topic>Enzyme Induction</topic><topic>Ethidium - pharmacology</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Genetic aspects</topic><topic>Health aspects</topic><topic>Humans</topic><topic>Intracellular Membranes - ultrastructure</topic><topic>Life sciences</topic><topic>Liver Neoplasms - pathology</topic><topic>Membrane Glycoproteins - antagonists & inhibitors</topic><topic>Membrane Glycoproteins - pharmacology</topic><topic>Membrane Glycoproteins - physiology</topic><topic>Membrane Potentials</topic><topic>Mitochondria</topic><topic>Mitochondria - physiology</topic><topic>Mitochondria - ultrastructure</topic><topic>Mitochondrial DNA</topic><topic>Molecular and cellular biology</topic><topic>Phosphorylation</topic><topic>Physiological aspects</topic><topic>Ploidy</topic><topic>Protein Transport</topic><topic>Proto-Oncogene Proteins - physiology</topic><topic>Proto-Oncogene Proteins c-bcl-2</topic><topic>Signal transduction</topic><topic>Staurosporine</topic><topic>TNF-Related Apoptosis-Inducing Ligand</topic><topic>Tumor cells</topic><topic>Tumor Cells, Cultured - drug effects</topic><topic>Tumor Cells, Cultured - metabolism</topic><topic>Tumor necrosis factor</topic><topic>Tumor Necrosis Factor-alpha - antagonists & inhibitors</topic><topic>Tumor Necrosis Factor-alpha - pharmacology</topic><topic>Tumor Necrosis Factor-alpha - physiology</topic><topic>Tumor necrosis factor-α</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>KIM, Ja-Young</creatorcontrib><creatorcontrib>KIM, Yun-Hee</creatorcontrib><creatorcontrib>INIK CHANG</creatorcontrib><creatorcontrib>SUNSHIN KIM</creatorcontrib><creatorcontrib>YOUNGMI KIM PAK</creatorcontrib><creatorcontrib>OH, Byung-Ha</creatorcontrib><creatorcontrib>YAGITA, Hideo</creatorcontrib><creatorcontrib>YONG KEUN JUNG</creatorcontrib><creatorcontrib>YOUNG JOON OH</creatorcontrib><creatorcontrib>LEE, Myung-Shik</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>ProQuest Central (Corporate)</collection><collection>Nucleic Acids Abstracts</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>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>Research Library (Alumni Edition)</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</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>Research Library Prep</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>Research Library</collection><collection>Biological Science Database</collection><collection>Research Library (Corporate)</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>ProQuest Central Basic</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Oncogene</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>KIM, Ja-Young</au><au>KIM, Yun-Hee</au><au>INIK CHANG</au><au>SUNSHIN KIM</au><au>YOUNGMI KIM PAK</au><au>OH, Byung-Ha</au><au>YAGITA, Hideo</au><au>YONG KEUN JUNG</au><au>YOUNG JOON OH</au><au>LEE, Myung-Shik</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Resistance of mitochondrial DNA-deficient cells to TRAIL: Role of Bax in TRAIL-induced apoptosis</atitle><jtitle>Oncogene</jtitle><addtitle>Oncogene</addtitle><date>2002-05-09</date><risdate>2002</risdate><volume>21</volume><issue>20</issue><spage>3139</spage><epage>3148</epage><pages>3139-3148</pages><issn>0950-9232</issn><eissn>1476-5594</eissn><coden>ONCNES</coden><abstract>Mitochondrion is one of the master players in both apoptosis and necrosis. We studied the role of mitochondrial function in TRAIL-induced apoptosis. TRAIL killed SK-Hep1 cells with characteristic features of apoptosis such as DNA fragmentation, sub-G1 ploidy peak and cytochrome c translocation. In contrast, mitochondrial DNA-deficient SK-Hep1 rho(0) cells were resistant to TRAIL. Dissipation of mitochondrial potential or cytochrome c translocation did not occur in rho(0) cells after TRAIL treatment. TRAIL induced translocation of Bax subsequent to the cleavage of Bid in parental cells. However, Bax translocation was absent in rho(0) cells, accounting for the failure of cytochrome c release in rho(0) cells. Forced expression of Bax induced caspase-3 activity in rho(0) cells. Incubation of rho(0) cells with ADP+Pi to increase intracellular ATP restored sensitivity to TRAIL. Despite different sensitivity to TRAIL, parental cells and rho(0) cells did not show significant difference in susceptibility to agonistic anti-Fas antibody, TNF-alpha or staurosporine. Our results indicate that TRAIL-induced apoptosis is dependent on intact mitochondrial function and susceptibility of mitochondrial DNA-deficient cells to apoptosis depends on the type of apoptotic stimuli. Tumor cells with mitochondrial mutations or dysfunction might have the ability to evade tumor surveillance imposed by TRAIL in vivo.</abstract><cop>Basingstoke</cop><pub>Nature Publishing</pub><pmid>12082629</pmid><doi>10.1038/sj.onc.1205406</doi><tpages>10</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0950-9232 |
| ispartof | Oncogene, 2002-05, Vol.21 (20), p.3139-3148 |
| issn | 0950-9232 1476-5594 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_71851227 |
| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Nature Journals Online; Alma/SFX Local Collection |
| subjects | Adenosine Triphosphate - physiology Ageing, cell death Apoptosis Apoptosis - drug effects Apoptosis - physiology Apoptosis Regulatory Proteins bcl-2-Associated X Protein BH3 Interacting Domain Death Agonist Protein Biological and medical sciences Cancer Carcinoma, Hepatocellular - pathology Carrier Proteins - metabolism Caspase 3 Caspase 8 Caspase 9 Caspases - biosynthesis Caspases - metabolism Cell death Cell physiology Cysteine Proteinase Inhibitors - pharmacology Cytochrome Cytochrome c Cytochrome c Group - metabolism DNA fragmentation DNA, Mitochondrial - drug effects DNA, Mitochondrial - physiology Enzyme Induction Ethidium - pharmacology Fundamental and applied biological sciences. Psychology Genetic aspects Health aspects Humans Intracellular Membranes - ultrastructure Life sciences Liver Neoplasms - pathology Membrane Glycoproteins - antagonists & inhibitors Membrane Glycoproteins - pharmacology Membrane Glycoproteins - physiology Membrane Potentials Mitochondria Mitochondria - physiology Mitochondria - ultrastructure Mitochondrial DNA Molecular and cellular biology Phosphorylation Physiological aspects Ploidy Protein Transport Proto-Oncogene Proteins - physiology Proto-Oncogene Proteins c-bcl-2 Signal transduction Staurosporine TNF-Related Apoptosis-Inducing Ligand Tumor cells Tumor Cells, Cultured - drug effects Tumor Cells, Cultured - metabolism Tumor necrosis factor Tumor Necrosis Factor-alpha - antagonists & inhibitors Tumor Necrosis Factor-alpha - pharmacology Tumor Necrosis Factor-alpha - physiology Tumor necrosis factor-α |
| title | Resistance of mitochondrial DNA-deficient cells to TRAIL: Role of Bax in TRAIL-induced apoptosis |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-18T05%3A56%3A19IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_proqu&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Resistance%20of%20mitochondrial%20DNA-deficient%20cells%20to%20TRAIL:%20Role%20of%20Bax%20in%20TRAIL-induced%20apoptosis&rft.jtitle=Oncogene&rft.au=KIM,%20Ja-Young&rft.date=2002-05-09&rft.volume=21&rft.issue=20&rft.spage=3139&rft.epage=3148&rft.pages=3139-3148&rft.issn=0950-9232&rft.eissn=1476-5594&rft.coden=ONCNES&rft_id=info:doi/10.1038/sj.onc.1205406&rft_dat=%3Cgale_proqu%3EA205597093%3C/gale_proqu%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=227312131&rft_id=info:pmid/12082629&rft_galeid=A205597093&rfr_iscdi=true |