Targeting Pro-Apoptotic TRAIL Receptors Sensitizes HeLa Cervical Cancer Cells to Irradiation-Induced Apoptosis
Purpose To investigate the potential of irradiation in combination with drugs targeting the tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) death receptor (DR)4 and DR5 and their mechanism of action in a cervical cancer cell line. Methods and Materials Recombinant human TRAIL (rhTRAI...
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| Veröffentlicht in: | International journal of radiation oncology, biology, physics biology, physics, 2008-10, Vol.72 (2), p.543-552 |
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| creator | Maduro, John H., M.D de Vries, Elisabeth G.E., M.D., Ph.D Meersma, Gert-Jan Hougardy, Brigitte M.T., Ph.D van der Zee, Ate G.J., M.D., Ph.D de Jong, Steven, Ph.D |
| description | Purpose To investigate the potential of irradiation in combination with drugs targeting the tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) death receptor (DR)4 and DR5 and their mechanism of action in a cervical cancer cell line. Methods and Materials Recombinant human TRAIL (rhTRAIL) and the agonistic antibodies against DR4 and DR5 were added to irradiated HeLa cells. The effect was evaluated with apoptosis and cytotoxicity assays and at the protein level. Membrane receptor expression was measured with flow cytometry. Small-interfering RNA against p53, DR4, and DR5 was used to investigate their function on the combined effect. Results rhTRAIL and the agonistic DR4 and DR5 antibodies strongly enhanced 10-Gy–induced apoptosis. This extra effect was 22%, 23%, and 29% for rhTRAIL, DR4, and DR5, respectively. Irradiation increased p53 expression and increased the membrane expression of DR5 and DR4. p53 suppression, as well as small-interfering RNA against DR5, resulted in a significant downregulation of DR5 membrane expression but did not affect apoptosis induced by irradiation and rhTRAIL. After small-interfering RNA against DR4, rhTRAIL-induced apoptosis and the additive effect of irradiation on rhTRAIL-induced apoptosis were abrogated, implicating an important role for DR4 in apoptosis induced through irradiation in combination with rhTRAIL. Conclusion Irradiation-induced apoptosis is strongly enhanced by targeting the pro-apoptotic TRAIL receptors DR4 or DR5. Irradiation results in a p53-dependent increase in DR5 membrane expression. The sensitizing effect of rhTRAIL on irradiation in the HeLa cell line is, however especially mediated through the DR4 receptor. |
| doi_str_mv | 10.1016/j.ijrobp.2008.06.1902 |
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| fullrecord | <record><control><sourceid>elsevier_osti_</sourceid><recordid>TN_cdi_osti_scitechconnect_21124483</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>1_s2_0_S0360301608025364</els_id><sourcerecordid>1_s2_0_S0360301608025364</sourcerecordid><originalsourceid>FETCH-LOGICAL-c446t-2539c2b5e7b038246ce6521811f171b0e91349ff86909a99132320ce6f060bd63</originalsourceid><addsrcrecordid>eNqFkVGL1DAQx4Mo3nr6EZSAz62TpM02L8qynN7CgnK3gm-hTadnai8pSfbg_PSm9EDwxacw4Tf_TH5DyFsGJQMmP4ylHYPv5pIDNCXIkingz8iGNVtViLr-8ZxsQEgoRKYvyKsYRwBgbFu9JBcLJFQtN8Sd2nCHybo7-i34Yjf7OflkDT3d7A5HeoMG80WI9BZdtMn-xkiv8djSPYYHa9qJ7ltnMOR6miJNnh5CaHvbJutdcXD92WBP19ho42vyYminiG-ezkvy_fPVaX9dHL9-Oex3x8JUlUwFr4UyvKtx24FoeCUNypqzhrGBbVkHqJio1DA0UoFqVa644JChASR0vRSX5P2a62OyOhqb0Pw03jk0SXPGeFU1IlP1SpngYww46DnY-zY8agZ6saxHvVrWi2UNUi-Wc9-7tW8-d_fY_-160pqBTyuA-Y8PFsMyAmZPvQ3LBL23_33i4z8JZrJuEf4LHzGO_hxcFqiZjlyDvl1WvWwaGsjyZCX-ABgLpAM</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype></control><display><type>article</type><title>Targeting Pro-Apoptotic TRAIL Receptors Sensitizes HeLa Cervical Cancer Cells to Irradiation-Induced Apoptosis</title><source>MEDLINE</source><source>ScienceDirect Journals (5 years ago - present)</source><creator>Maduro, John H., M.D ; de Vries, Elisabeth G.E., M.D., Ph.D ; Meersma, Gert-Jan ; Hougardy, Brigitte M.T., Ph.D ; van der Zee, Ate G.J., M.D., Ph.D ; de Jong, Steven, Ph.D</creator><creatorcontrib>Maduro, John H., M.D ; de Vries, Elisabeth G.E., M.D., Ph.D ; Meersma, Gert-Jan ; Hougardy, Brigitte M.T., Ph.D ; van der Zee, Ate G.J., M.D., Ph.D ; de Jong, Steven, Ph.D</creatorcontrib><description>Purpose To investigate the potential of irradiation in combination with drugs targeting the tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) death receptor (DR)4 and DR5 and their mechanism of action in a cervical cancer cell line. Methods and Materials Recombinant human TRAIL (rhTRAIL) and the agonistic antibodies against DR4 and DR5 were added to irradiated HeLa cells. The effect was evaluated with apoptosis and cytotoxicity assays and at the protein level. Membrane receptor expression was measured with flow cytometry. Small-interfering RNA against p53, DR4, and DR5 was used to investigate their function on the combined effect. Results rhTRAIL and the agonistic DR4 and DR5 antibodies strongly enhanced 10-Gy–induced apoptosis. This extra effect was 22%, 23%, and 29% for rhTRAIL, DR4, and DR5, respectively. Irradiation increased p53 expression and increased the membrane expression of DR5 and DR4. p53 suppression, as well as small-interfering RNA against DR5, resulted in a significant downregulation of DR5 membrane expression but did not affect apoptosis induced by irradiation and rhTRAIL. After small-interfering RNA against DR4, rhTRAIL-induced apoptosis and the additive effect of irradiation on rhTRAIL-induced apoptosis were abrogated, implicating an important role for DR4 in apoptosis induced through irradiation in combination with rhTRAIL. Conclusion Irradiation-induced apoptosis is strongly enhanced by targeting the pro-apoptotic TRAIL receptors DR4 or DR5. Irradiation results in a p53-dependent increase in DR5 membrane expression. The sensitizing effect of rhTRAIL on irradiation in the HeLa cell line is, however especially mediated through the DR4 receptor.</description><identifier>ISSN: 0360-3016</identifier><identifier>EISSN: 1879-355X</identifier><identifier>DOI: 10.1016/j.ijrobp.2008.06.1902</identifier><identifier>PMID: 18793956</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>ANTIBODIES ; APOPTOSIS ; Apoptosis - drug effects ; Apoptosis - radiation effects ; CARCINOMAS ; Caspase 3 - metabolism ; Cell Survival - drug effects ; Cell Survival - radiation effects ; Cervical cancer ; Collagen Type XI - metabolism ; Combined Modality Therapy - methods ; DEATH ; Death receptors ; Drug Screening Assays, Antitumor ; DRUGS ; Enzyme Activation ; Female ; HELA CELLS ; HeLa Cells - drug effects ; HeLa Cells - radiation effects ; Hematology, Oncology and Palliative Medicine ; Humans ; IRRADIATION ; LIGANDS ; Neoplasm Proteins - drug effects ; Neoplasm Proteins - metabolism ; Neoplasm Proteins - radiation effects ; Radiation Dosage ; Radiation Tolerance ; Radiology ; RADIOLOGY AND NUCLEAR MEDICINE ; RECEPTORS ; Receptors, TNF-Related Apoptosis-Inducing Ligand - drug effects ; Receptors, TNF-Related Apoptosis-Inducing Ligand - metabolism ; Receptors, TNF-Related Apoptosis-Inducing Ligand - radiation effects ; Receptors, Tumor Necrosis Factor - drug effects ; Receptors, Tumor Necrosis Factor - metabolism ; Recombinant Proteins - pharmacology ; RNA ; RNA, Small Interfering - metabolism ; TNF-Related Apoptosis-Inducing Ligand - pharmacology ; TOXICITY ; TRAIL ; Tumor necrosis factor-related apoptosis-inducing ligand ; Tumor Suppressor Protein p53 - metabolism ; Tumor Suppressor Protein p53 - radiation effects ; Uterine Cervical Neoplasms - drug therapy ; Uterine Cervical Neoplasms - metabolism ; Uterine Cervical Neoplasms - radiotherapy</subject><ispartof>International journal of radiation oncology, biology, physics, 2008-10, Vol.72 (2), p.543-552</ispartof><rights>Elsevier Inc.</rights><rights>2008 Elsevier Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c446t-2539c2b5e7b038246ce6521811f171b0e91349ff86909a99132320ce6f060bd63</citedby><cites>FETCH-LOGICAL-c446t-2539c2b5e7b038246ce6521811f171b0e91349ff86909a99132320ce6f060bd63</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.ijrobp.2008.06.1902$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>230,314,780,784,885,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18793956$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://www.osti.gov/biblio/21124483$$D View this record in Osti.gov$$Hfree_for_read</backlink></links><search><creatorcontrib>Maduro, John H., M.D</creatorcontrib><creatorcontrib>de Vries, Elisabeth G.E., M.D., Ph.D</creatorcontrib><creatorcontrib>Meersma, Gert-Jan</creatorcontrib><creatorcontrib>Hougardy, Brigitte M.T., Ph.D</creatorcontrib><creatorcontrib>van der Zee, Ate G.J., M.D., Ph.D</creatorcontrib><creatorcontrib>de Jong, Steven, Ph.D</creatorcontrib><title>Targeting Pro-Apoptotic TRAIL Receptors Sensitizes HeLa Cervical Cancer Cells to Irradiation-Induced Apoptosis</title><title>International journal of radiation oncology, biology, physics</title><addtitle>Int J Radiat Oncol Biol Phys</addtitle><description>Purpose To investigate the potential of irradiation in combination with drugs targeting the tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) death receptor (DR)4 and DR5 and their mechanism of action in a cervical cancer cell line. Methods and Materials Recombinant human TRAIL (rhTRAIL) and the agonistic antibodies against DR4 and DR5 were added to irradiated HeLa cells. The effect was evaluated with apoptosis and cytotoxicity assays and at the protein level. Membrane receptor expression was measured with flow cytometry. Small-interfering RNA against p53, DR4, and DR5 was used to investigate their function on the combined effect. Results rhTRAIL and the agonistic DR4 and DR5 antibodies strongly enhanced 10-Gy–induced apoptosis. This extra effect was 22%, 23%, and 29% for rhTRAIL, DR4, and DR5, respectively. Irradiation increased p53 expression and increased the membrane expression of DR5 and DR4. p53 suppression, as well as small-interfering RNA against DR5, resulted in a significant downregulation of DR5 membrane expression but did not affect apoptosis induced by irradiation and rhTRAIL. After small-interfering RNA against DR4, rhTRAIL-induced apoptosis and the additive effect of irradiation on rhTRAIL-induced apoptosis were abrogated, implicating an important role for DR4 in apoptosis induced through irradiation in combination with rhTRAIL. Conclusion Irradiation-induced apoptosis is strongly enhanced by targeting the pro-apoptotic TRAIL receptors DR4 or DR5. Irradiation results in a p53-dependent increase in DR5 membrane expression. The sensitizing effect of rhTRAIL on irradiation in the HeLa cell line is, however especially mediated through the DR4 receptor.</description><subject>ANTIBODIES</subject><subject>APOPTOSIS</subject><subject>Apoptosis - drug effects</subject><subject>Apoptosis - radiation effects</subject><subject>CARCINOMAS</subject><subject>Caspase 3 - metabolism</subject><subject>Cell Survival - drug effects</subject><subject>Cell Survival - radiation effects</subject><subject>Cervical cancer</subject><subject>Collagen Type XI - metabolism</subject><subject>Combined Modality Therapy - methods</subject><subject>DEATH</subject><subject>Death receptors</subject><subject>Drug Screening Assays, Antitumor</subject><subject>DRUGS</subject><subject>Enzyme Activation</subject><subject>Female</subject><subject>HELA CELLS</subject><subject>HeLa Cells - drug effects</subject><subject>HeLa Cells - radiation effects</subject><subject>Hematology, Oncology and Palliative Medicine</subject><subject>Humans</subject><subject>IRRADIATION</subject><subject>LIGANDS</subject><subject>Neoplasm Proteins - drug effects</subject><subject>Neoplasm Proteins - metabolism</subject><subject>Neoplasm Proteins - radiation effects</subject><subject>Radiation Dosage</subject><subject>Radiation Tolerance</subject><subject>Radiology</subject><subject>RADIOLOGY AND NUCLEAR MEDICINE</subject><subject>RECEPTORS</subject><subject>Receptors, TNF-Related Apoptosis-Inducing Ligand - drug effects</subject><subject>Receptors, TNF-Related Apoptosis-Inducing Ligand - metabolism</subject><subject>Receptors, TNF-Related Apoptosis-Inducing Ligand - radiation effects</subject><subject>Receptors, Tumor Necrosis Factor - drug effects</subject><subject>Receptors, Tumor Necrosis Factor - metabolism</subject><subject>Recombinant Proteins - pharmacology</subject><subject>RNA</subject><subject>RNA, Small Interfering - metabolism</subject><subject>TNF-Related Apoptosis-Inducing Ligand - pharmacology</subject><subject>TOXICITY</subject><subject>TRAIL</subject><subject>Tumor necrosis factor-related apoptosis-inducing ligand</subject><subject>Tumor Suppressor Protein p53 - metabolism</subject><subject>Tumor Suppressor Protein p53 - radiation effects</subject><subject>Uterine Cervical Neoplasms - drug therapy</subject><subject>Uterine Cervical Neoplasms - metabolism</subject><subject>Uterine Cervical Neoplasms - radiotherapy</subject><issn>0360-3016</issn><issn>1879-355X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkVGL1DAQx4Mo3nr6EZSAz62TpM02L8qynN7CgnK3gm-hTadnai8pSfbg_PSm9EDwxacw4Tf_TH5DyFsGJQMmP4ylHYPv5pIDNCXIkingz8iGNVtViLr-8ZxsQEgoRKYvyKsYRwBgbFu9JBcLJFQtN8Sd2nCHybo7-i34Yjf7OflkDT3d7A5HeoMG80WI9BZdtMn-xkiv8djSPYYHa9qJ7ltnMOR6miJNnh5CaHvbJutdcXD92WBP19ho42vyYminiG-ezkvy_fPVaX9dHL9-Oex3x8JUlUwFr4UyvKtx24FoeCUNypqzhrGBbVkHqJio1DA0UoFqVa644JChASR0vRSX5P2a62OyOhqb0Pw03jk0SXPGeFU1IlP1SpngYww46DnY-zY8agZ6saxHvVrWi2UNUi-Wc9-7tW8-d_fY_-160pqBTyuA-Y8PFsMyAmZPvQ3LBL23_33i4z8JZrJuEf4LHzGO_hxcFqiZjlyDvl1WvWwaGsjyZCX-ABgLpAM</recordid><startdate>20081001</startdate><enddate>20081001</enddate><creator>Maduro, John H., M.D</creator><creator>de Vries, Elisabeth G.E., M.D., Ph.D</creator><creator>Meersma, Gert-Jan</creator><creator>Hougardy, Brigitte M.T., Ph.D</creator><creator>van der Zee, Ate G.J., M.D., Ph.D</creator><creator>de Jong, Steven, Ph.D</creator><general>Elsevier Inc</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>OTOTI</scope></search><sort><creationdate>20081001</creationdate><title>Targeting Pro-Apoptotic TRAIL Receptors Sensitizes HeLa Cervical Cancer Cells to Irradiation-Induced Apoptosis</title><author>Maduro, John H., M.D ; de Vries, Elisabeth G.E., M.D., Ph.D ; Meersma, Gert-Jan ; Hougardy, Brigitte M.T., Ph.D ; van der Zee, Ate G.J., M.D., Ph.D ; de Jong, Steven, Ph.D</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c446t-2539c2b5e7b038246ce6521811f171b0e91349ff86909a99132320ce6f060bd63</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>ANTIBODIES</topic><topic>APOPTOSIS</topic><topic>Apoptosis - drug effects</topic><topic>Apoptosis - radiation effects</topic><topic>CARCINOMAS</topic><topic>Caspase 3 - metabolism</topic><topic>Cell Survival - drug effects</topic><topic>Cell Survival - radiation effects</topic><topic>Cervical cancer</topic><topic>Collagen Type XI - metabolism</topic><topic>Combined Modality Therapy - methods</topic><topic>DEATH</topic><topic>Death receptors</topic><topic>Drug Screening Assays, Antitumor</topic><topic>DRUGS</topic><topic>Enzyme Activation</topic><topic>Female</topic><topic>HELA CELLS</topic><topic>HeLa Cells - drug effects</topic><topic>HeLa Cells - radiation effects</topic><topic>Hematology, Oncology and Palliative Medicine</topic><topic>Humans</topic><topic>IRRADIATION</topic><topic>LIGANDS</topic><topic>Neoplasm Proteins - drug effects</topic><topic>Neoplasm Proteins - metabolism</topic><topic>Neoplasm Proteins - radiation effects</topic><topic>Radiation Dosage</topic><topic>Radiation Tolerance</topic><topic>Radiology</topic><topic>RADIOLOGY AND NUCLEAR MEDICINE</topic><topic>RECEPTORS</topic><topic>Receptors, TNF-Related Apoptosis-Inducing Ligand - drug effects</topic><topic>Receptors, TNF-Related Apoptosis-Inducing Ligand - metabolism</topic><topic>Receptors, TNF-Related Apoptosis-Inducing Ligand - radiation effects</topic><topic>Receptors, Tumor Necrosis Factor - drug effects</topic><topic>Receptors, Tumor Necrosis Factor - metabolism</topic><topic>Recombinant Proteins - pharmacology</topic><topic>RNA</topic><topic>RNA, Small Interfering - metabolism</topic><topic>TNF-Related Apoptosis-Inducing Ligand - pharmacology</topic><topic>TOXICITY</topic><topic>TRAIL</topic><topic>Tumor necrosis factor-related apoptosis-inducing ligand</topic><topic>Tumor Suppressor Protein p53 - metabolism</topic><topic>Tumor Suppressor Protein p53 - radiation effects</topic><topic>Uterine Cervical Neoplasms - drug therapy</topic><topic>Uterine Cervical Neoplasms - metabolism</topic><topic>Uterine Cervical Neoplasms - radiotherapy</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Maduro, John H., M.D</creatorcontrib><creatorcontrib>de Vries, Elisabeth G.E., M.D., Ph.D</creatorcontrib><creatorcontrib>Meersma, Gert-Jan</creatorcontrib><creatorcontrib>Hougardy, Brigitte M.T., Ph.D</creatorcontrib><creatorcontrib>van der Zee, Ate G.J., M.D., Ph.D</creatorcontrib><creatorcontrib>de Jong, Steven, Ph.D</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>OSTI.GOV</collection><jtitle>International journal of radiation oncology, biology, physics</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Maduro, John H., M.D</au><au>de Vries, Elisabeth G.E., M.D., Ph.D</au><au>Meersma, Gert-Jan</au><au>Hougardy, Brigitte M.T., Ph.D</au><au>van der Zee, Ate G.J., M.D., Ph.D</au><au>de Jong, Steven, Ph.D</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Targeting Pro-Apoptotic TRAIL Receptors Sensitizes HeLa Cervical Cancer Cells to Irradiation-Induced Apoptosis</atitle><jtitle>International journal of radiation oncology, biology, physics</jtitle><addtitle>Int J Radiat Oncol Biol Phys</addtitle><date>2008-10-01</date><risdate>2008</risdate><volume>72</volume><issue>2</issue><spage>543</spage><epage>552</epage><pages>543-552</pages><issn>0360-3016</issn><eissn>1879-355X</eissn><abstract>Purpose To investigate the potential of irradiation in combination with drugs targeting the tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) death receptor (DR)4 and DR5 and their mechanism of action in a cervical cancer cell line. Methods and Materials Recombinant human TRAIL (rhTRAIL) and the agonistic antibodies against DR4 and DR5 were added to irradiated HeLa cells. The effect was evaluated with apoptosis and cytotoxicity assays and at the protein level. Membrane receptor expression was measured with flow cytometry. Small-interfering RNA against p53, DR4, and DR5 was used to investigate their function on the combined effect. Results rhTRAIL and the agonistic DR4 and DR5 antibodies strongly enhanced 10-Gy–induced apoptosis. This extra effect was 22%, 23%, and 29% for rhTRAIL, DR4, and DR5, respectively. Irradiation increased p53 expression and increased the membrane expression of DR5 and DR4. p53 suppression, as well as small-interfering RNA against DR5, resulted in a significant downregulation of DR5 membrane expression but did not affect apoptosis induced by irradiation and rhTRAIL. After small-interfering RNA against DR4, rhTRAIL-induced apoptosis and the additive effect of irradiation on rhTRAIL-induced apoptosis were abrogated, implicating an important role for DR4 in apoptosis induced through irradiation in combination with rhTRAIL. Conclusion Irradiation-induced apoptosis is strongly enhanced by targeting the pro-apoptotic TRAIL receptors DR4 or DR5. Irradiation results in a p53-dependent increase in DR5 membrane expression. The sensitizing effect of rhTRAIL on irradiation in the HeLa cell line is, however especially mediated through the DR4 receptor.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>18793956</pmid><doi>10.1016/j.ijrobp.2008.06.1902</doi><tpages>10</tpages></addata></record> |
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| identifier | ISSN: 0360-3016 |
| ispartof | International journal of radiation oncology, biology, physics, 2008-10, Vol.72 (2), p.543-552 |
| issn | 0360-3016 1879-355X |
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| subjects | ANTIBODIES APOPTOSIS Apoptosis - drug effects Apoptosis - radiation effects CARCINOMAS Caspase 3 - metabolism Cell Survival - drug effects Cell Survival - radiation effects Cervical cancer Collagen Type XI - metabolism Combined Modality Therapy - methods DEATH Death receptors Drug Screening Assays, Antitumor DRUGS Enzyme Activation Female HELA CELLS HeLa Cells - drug effects HeLa Cells - radiation effects Hematology, Oncology and Palliative Medicine Humans IRRADIATION LIGANDS Neoplasm Proteins - drug effects Neoplasm Proteins - metabolism Neoplasm Proteins - radiation effects Radiation Dosage Radiation Tolerance Radiology RADIOLOGY AND NUCLEAR MEDICINE RECEPTORS Receptors, TNF-Related Apoptosis-Inducing Ligand - drug effects Receptors, TNF-Related Apoptosis-Inducing Ligand - metabolism Receptors, TNF-Related Apoptosis-Inducing Ligand - radiation effects Receptors, Tumor Necrosis Factor - drug effects Receptors, Tumor Necrosis Factor - metabolism Recombinant Proteins - pharmacology RNA RNA, Small Interfering - metabolism TNF-Related Apoptosis-Inducing Ligand - pharmacology TOXICITY TRAIL Tumor necrosis factor-related apoptosis-inducing ligand Tumor Suppressor Protein p53 - metabolism Tumor Suppressor Protein p53 - radiation effects Uterine Cervical Neoplasms - drug therapy Uterine Cervical Neoplasms - metabolism Uterine Cervical Neoplasms - radiotherapy |
| title | Targeting Pro-Apoptotic TRAIL Receptors Sensitizes HeLa Cervical Cancer Cells to Irradiation-Induced Apoptosis |
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