Effects of sequential treatments with chemotherapeutic drugs followed by TRAIL on prostate cancer in vitro and in vivo
BACKGROUND Tumor necrosis factor related apoptosis‐inducing ligand/Apo2 ligand (TRAIL/Apo‐2L) is a novel anticancer agent, capable of inducing apoptosis preferentially in tumor and transformed cells. TRAIL‐R1/death receptor (DR)4 and TRAIL‐R2/DR5 are members of the tumor necrosis factor (TNF) recept...
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| Veröffentlicht in: | The Prostate 2005-02, Vol.62 (2), p.165-186 |
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| creator | Shankar, Sharmila Chen, Xufen Srivastava, Rakesh K. |
| description | BACKGROUND
Tumor necrosis factor related apoptosis‐inducing ligand/Apo2 ligand (TRAIL/Apo‐2L) is a novel anticancer agent, capable of inducing apoptosis preferentially in tumor and transformed cells. TRAIL‐R1/death receptor (DR)4 and TRAIL‐R2/DR5 are members of the tumor necrosis factor (TNF) receptor family, and can be activated by the TRAIL. We examined the clinical potential of chemotherapeutic drugs and TRAIL for the treatment of prostate cancer.
METHODS
Prostate and bladder cancer cells were exposed to chemotherapeutic drugs (paclitaxel, vincristine, vinblastine, etoposide, doxorubicin, and camptothecin) and TRAIL. Cell viability was measured by sodium 3′[1‐(phenylaminocarbonyl)‐3,4‐tetrazolium]‐bis (4‐methoxy‐6‐nitro) assay; expressions of death receptors and Bcl‐2 family members were measured by Western blotting, ELISA and ribonuclease protection assay. PC‐3 tumor cells xenografted athymic nude mice were exposed to chemotherapeutic drugs and TRAIL, either alone or in combination, to measure tumor growth and survival of mice. Apoptosis was measured by annexin V–FITC/propidium iodide staining, and terminal deoxynucleotidyltransferase‐mediated nick end labeling assay. Caspase‐3 activity was measured by the Western blotting and immunohistochemistry.
RESULTS
TRAIL induced apoptosis with varying sensitivity. Chemotherapeutic drugs (paclitaxel, vincristine, vinblastine, etoposide, doxorubicin, and camptothecin) significantly augmented TRAIL‐induced apoptosis in cancer cells through up‐regulation of DR4, DR5, Bax, and Bak, and induction of caspase activation. Mitochondrial pathway enhanced the synergistic interactions between drugs and TRAIL. The sequential treatment of mice with chemotherapeutic drugs followed by TRAIL induced caspase‐3 activity, and apoptosis, inhibited angiogenesis, completely eradicated the established tumors, and enhanced survival of mice.
CONCLUSIONS
Chemotherapeutic drugs can be used to enhance the therapeutic potential of TRAIL in prostate cancer. © 2004 Wiley‐Liss, Inc. |
| doi_str_mv | 10.1002/pros.20126 |
| format | Article |
| fullrecord | <record><control><sourceid>wiley_cross</sourceid><recordid>TN_cdi_crossref_primary_10_1002_pros_20126</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>PROS20126</sourcerecordid><originalsourceid>FETCH-LOGICAL-c3956-20045bc29eda4cf6eb38b5efb01bc38a52d4277d642521418071c291c0569ea3</originalsourceid><addsrcrecordid>eNp90E1vEzEQBmALgWgoXPgByBculbaMv9a7x6pqSqWIohIJqRfL6x0Tw2Y32E5C_j0bNtAbJ2ukZzwzLyFvGVwyAP5hE4d0yYHx8hmZMah1ASDVczIDrqGQTOgz8iql7wAjB_6SnDElqroCNiO7G-_R5UQHTxP-3GKfg-1ojmjzeiwS3Ye8om6F6yGvMNoNbnNwtI3bb4n6oeuGPba0OdDlw9Xdgg49Pa6TbUbqbO8w0tDTXchxoLZvp2I3vCYvvO0Svjm952Q5v1lefywW97d311eLwolalQU_HtI4XmNrpfMlNqJqFPoGWONEZRVvJde6LSVXnElWgWajZg5UWaMV5-Ri-taNO6WI3mxiWNt4MAzMMTtzXNb8yW7E7ya82TZrbJ_oKawRvD8Bm5ztfBzvC-nJlUrIWurRscntQ4eH_4w0nx_uv_wdXkw9IWX89a_Hxh-m1EIr8_XTrXmci0ou56V5FL8B-KWXMw</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype></control><display><type>article</type><title>Effects of sequential treatments with chemotherapeutic drugs followed by TRAIL on prostate cancer in vitro and in vivo</title><source>MEDLINE</source><source>Wiley Online Library Journals Frontfile Complete</source><creator>Shankar, Sharmila ; Chen, Xufen ; Srivastava, Rakesh K.</creator><creatorcontrib>Shankar, Sharmila ; Chen, Xufen ; Srivastava, Rakesh K.</creatorcontrib><description>BACKGROUND
Tumor necrosis factor related apoptosis‐inducing ligand/Apo2 ligand (TRAIL/Apo‐2L) is a novel anticancer agent, capable of inducing apoptosis preferentially in tumor and transformed cells. TRAIL‐R1/death receptor (DR)4 and TRAIL‐R2/DR5 are members of the tumor necrosis factor (TNF) receptor family, and can be activated by the TRAIL. We examined the clinical potential of chemotherapeutic drugs and TRAIL for the treatment of prostate cancer.
METHODS
Prostate and bladder cancer cells were exposed to chemotherapeutic drugs (paclitaxel, vincristine, vinblastine, etoposide, doxorubicin, and camptothecin) and TRAIL. Cell viability was measured by sodium 3′[1‐(phenylaminocarbonyl)‐3,4‐tetrazolium]‐bis (4‐methoxy‐6‐nitro) assay; expressions of death receptors and Bcl‐2 family members were measured by Western blotting, ELISA and ribonuclease protection assay. PC‐3 tumor cells xenografted athymic nude mice were exposed to chemotherapeutic drugs and TRAIL, either alone or in combination, to measure tumor growth and survival of mice. Apoptosis was measured by annexin V–FITC/propidium iodide staining, and terminal deoxynucleotidyltransferase‐mediated nick end labeling assay. Caspase‐3 activity was measured by the Western blotting and immunohistochemistry.
RESULTS
TRAIL induced apoptosis with varying sensitivity. Chemotherapeutic drugs (paclitaxel, vincristine, vinblastine, etoposide, doxorubicin, and camptothecin) significantly augmented TRAIL‐induced apoptosis in cancer cells through up‐regulation of DR4, DR5, Bax, and Bak, and induction of caspase activation. Mitochondrial pathway enhanced the synergistic interactions between drugs and TRAIL. The sequential treatment of mice with chemotherapeutic drugs followed by TRAIL induced caspase‐3 activity, and apoptosis, inhibited angiogenesis, completely eradicated the established tumors, and enhanced survival of mice.
CONCLUSIONS
Chemotherapeutic drugs can be used to enhance the therapeutic potential of TRAIL in prostate cancer. © 2004 Wiley‐Liss, Inc.</description><identifier>ISSN: 0270-4137</identifier><identifier>EISSN: 1097-0045</identifier><identifier>DOI: 10.1002/pros.20126</identifier><identifier>PMID: 15389801</identifier><identifier>CODEN: PRSTDS</identifier><language>eng</language><publisher>Hoboken: Wiley Subscription Services, Inc., A Wiley Company</publisher><subject>Androgens - metabolism ; Animals ; Antineoplastic Agents - pharmacology ; apoptosis ; Apoptosis - drug effects ; Apoptosis Regulatory Proteins ; Biological and medical sciences ; Caspase 3 ; Caspases - metabolism ; chemotherapy ; death receptors ; Drug Synergism ; Gynecology. Andrology. Obstetrics ; Humans ; In Vitro Techniques ; Male ; Medical sciences ; Membrane Glycoproteins - pharmacology ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; Mitochondria - drug effects ; Mitochondria - physiology ; Neovascularization, Pathologic - drug therapy ; Neovascularization, Pathologic - mortality ; Nephrology. Urinary tract diseases ; prostate cancer ; Prostatic Neoplasms - drug therapy ; Prostatic Neoplasms - mortality ; Proto-Oncogene Proteins c-bcl-2 - metabolism ; Receptors, TNF-Related Apoptosis-Inducing Ligand ; Receptors, Tumor Necrosis Factor - metabolism ; Survival Rate ; TNF-Related Apoptosis-Inducing Ligand ; TRAIL/Apo-2L ; Tumor Necrosis Factor-alpha - pharmacology ; Tumors of the urinary system ; Urinary Bladder Neoplasms ; Urinary tract. Prostate gland</subject><ispartof>The Prostate, 2005-02, Vol.62 (2), p.165-186</ispartof><rights>Copyright © 2004 Wiley‐Liss, Inc.</rights><rights>2005 INIST-CNRS</rights><rights>Copyright 2004 Wiley-Liss, Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3956-20045bc29eda4cf6eb38b5efb01bc38a52d4277d642521418071c291c0569ea3</citedby><cites>FETCH-LOGICAL-c3956-20045bc29eda4cf6eb38b5efb01bc38a52d4277d642521418071c291c0569ea3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fpros.20126$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fpros.20126$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=16534947$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15389801$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Shankar, Sharmila</creatorcontrib><creatorcontrib>Chen, Xufen</creatorcontrib><creatorcontrib>Srivastava, Rakesh K.</creatorcontrib><title>Effects of sequential treatments with chemotherapeutic drugs followed by TRAIL on prostate cancer in vitro and in vivo</title><title>The Prostate</title><addtitle>Prostate</addtitle><description>BACKGROUND
Tumor necrosis factor related apoptosis‐inducing ligand/Apo2 ligand (TRAIL/Apo‐2L) is a novel anticancer agent, capable of inducing apoptosis preferentially in tumor and transformed cells. TRAIL‐R1/death receptor (DR)4 and TRAIL‐R2/DR5 are members of the tumor necrosis factor (TNF) receptor family, and can be activated by the TRAIL. We examined the clinical potential of chemotherapeutic drugs and TRAIL for the treatment of prostate cancer.
METHODS
Prostate and bladder cancer cells were exposed to chemotherapeutic drugs (paclitaxel, vincristine, vinblastine, etoposide, doxorubicin, and camptothecin) and TRAIL. Cell viability was measured by sodium 3′[1‐(phenylaminocarbonyl)‐3,4‐tetrazolium]‐bis (4‐methoxy‐6‐nitro) assay; expressions of death receptors and Bcl‐2 family members were measured by Western blotting, ELISA and ribonuclease protection assay. PC‐3 tumor cells xenografted athymic nude mice were exposed to chemotherapeutic drugs and TRAIL, either alone or in combination, to measure tumor growth and survival of mice. Apoptosis was measured by annexin V–FITC/propidium iodide staining, and terminal deoxynucleotidyltransferase‐mediated nick end labeling assay. Caspase‐3 activity was measured by the Western blotting and immunohistochemistry.
RESULTS
TRAIL induced apoptosis with varying sensitivity. Chemotherapeutic drugs (paclitaxel, vincristine, vinblastine, etoposide, doxorubicin, and camptothecin) significantly augmented TRAIL‐induced apoptosis in cancer cells through up‐regulation of DR4, DR5, Bax, and Bak, and induction of caspase activation. Mitochondrial pathway enhanced the synergistic interactions between drugs and TRAIL. The sequential treatment of mice with chemotherapeutic drugs followed by TRAIL induced caspase‐3 activity, and apoptosis, inhibited angiogenesis, completely eradicated the established tumors, and enhanced survival of mice.
CONCLUSIONS
Chemotherapeutic drugs can be used to enhance the therapeutic potential of TRAIL in prostate cancer. © 2004 Wiley‐Liss, Inc.</description><subject>Androgens - metabolism</subject><subject>Animals</subject><subject>Antineoplastic Agents - pharmacology</subject><subject>apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Apoptosis Regulatory Proteins</subject><subject>Biological and medical sciences</subject><subject>Caspase 3</subject><subject>Caspases - metabolism</subject><subject>chemotherapy</subject><subject>death receptors</subject><subject>Drug Synergism</subject><subject>Gynecology. Andrology. Obstetrics</subject><subject>Humans</subject><subject>In Vitro Techniques</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Membrane Glycoproteins - pharmacology</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Mice, Nude</subject><subject>Mitochondria - drug effects</subject><subject>Mitochondria - physiology</subject><subject>Neovascularization, Pathologic - drug therapy</subject><subject>Neovascularization, Pathologic - mortality</subject><subject>Nephrology. Urinary tract diseases</subject><subject>prostate cancer</subject><subject>Prostatic Neoplasms - drug therapy</subject><subject>Prostatic Neoplasms - mortality</subject><subject>Proto-Oncogene Proteins c-bcl-2 - metabolism</subject><subject>Receptors, TNF-Related Apoptosis-Inducing Ligand</subject><subject>Receptors, Tumor Necrosis Factor - metabolism</subject><subject>Survival Rate</subject><subject>TNF-Related Apoptosis-Inducing Ligand</subject><subject>TRAIL/Apo-2L</subject><subject>Tumor Necrosis Factor-alpha - pharmacology</subject><subject>Tumors of the urinary system</subject><subject>Urinary Bladder Neoplasms</subject><subject>Urinary tract. Prostate gland</subject><issn>0270-4137</issn><issn>1097-0045</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp90E1vEzEQBmALgWgoXPgByBculbaMv9a7x6pqSqWIohIJqRfL6x0Tw2Y32E5C_j0bNtAbJ2ukZzwzLyFvGVwyAP5hE4d0yYHx8hmZMah1ASDVczIDrqGQTOgz8iql7wAjB_6SnDElqroCNiO7G-_R5UQHTxP-3GKfg-1ojmjzeiwS3Ye8om6F6yGvMNoNbnNwtI3bb4n6oeuGPba0OdDlw9Xdgg49Pa6TbUbqbO8w0tDTXchxoLZvp2I3vCYvvO0Svjm952Q5v1lefywW97d311eLwolalQU_HtI4XmNrpfMlNqJqFPoGWONEZRVvJde6LSVXnElWgWajZg5UWaMV5-Ri-taNO6WI3mxiWNt4MAzMMTtzXNb8yW7E7ya82TZrbJ_oKawRvD8Bm5ztfBzvC-nJlUrIWurRscntQ4eH_4w0nx_uv_wdXkw9IWX89a_Hxh-m1EIr8_XTrXmci0ou56V5FL8B-KWXMw</recordid><startdate>20050201</startdate><enddate>20050201</enddate><creator>Shankar, Sharmila</creator><creator>Chen, Xufen</creator><creator>Srivastava, Rakesh K.</creator><general>Wiley Subscription Services, Inc., A Wiley Company</general><general>Wiley-Liss</general><scope>BSCLL</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></search><sort><creationdate>20050201</creationdate><title>Effects of sequential treatments with chemotherapeutic drugs followed by TRAIL on prostate cancer in vitro and in vivo</title><author>Shankar, Sharmila ; Chen, Xufen ; Srivastava, Rakesh K.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3956-20045bc29eda4cf6eb38b5efb01bc38a52d4277d642521418071c291c0569ea3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Androgens - metabolism</topic><topic>Animals</topic><topic>Antineoplastic Agents - pharmacology</topic><topic>apoptosis</topic><topic>Apoptosis - drug effects</topic><topic>Apoptosis Regulatory Proteins</topic><topic>Biological and medical sciences</topic><topic>Caspase 3</topic><topic>Caspases - metabolism</topic><topic>chemotherapy</topic><topic>death receptors</topic><topic>Drug Synergism</topic><topic>Gynecology. Andrology. Obstetrics</topic><topic>Humans</topic><topic>In Vitro Techniques</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Membrane Glycoproteins - pharmacology</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Mice, Nude</topic><topic>Mitochondria - drug effects</topic><topic>Mitochondria - physiology</topic><topic>Neovascularization, Pathologic - drug therapy</topic><topic>Neovascularization, Pathologic - mortality</topic><topic>Nephrology. Urinary tract diseases</topic><topic>prostate cancer</topic><topic>Prostatic Neoplasms - drug therapy</topic><topic>Prostatic Neoplasms - mortality</topic><topic>Proto-Oncogene Proteins c-bcl-2 - metabolism</topic><topic>Receptors, TNF-Related Apoptosis-Inducing Ligand</topic><topic>Receptors, Tumor Necrosis Factor - metabolism</topic><topic>Survival Rate</topic><topic>TNF-Related Apoptosis-Inducing Ligand</topic><topic>TRAIL/Apo-2L</topic><topic>Tumor Necrosis Factor-alpha - pharmacology</topic><topic>Tumors of the urinary system</topic><topic>Urinary Bladder Neoplasms</topic><topic>Urinary tract. Prostate gland</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Shankar, Sharmila</creatorcontrib><creatorcontrib>Chen, Xufen</creatorcontrib><creatorcontrib>Srivastava, Rakesh K.</creatorcontrib><collection>Istex</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><jtitle>The Prostate</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Shankar, Sharmila</au><au>Chen, Xufen</au><au>Srivastava, Rakesh K.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effects of sequential treatments with chemotherapeutic drugs followed by TRAIL on prostate cancer in vitro and in vivo</atitle><jtitle>The Prostate</jtitle><addtitle>Prostate</addtitle><date>2005-02-01</date><risdate>2005</risdate><volume>62</volume><issue>2</issue><spage>165</spage><epage>186</epage><pages>165-186</pages><issn>0270-4137</issn><eissn>1097-0045</eissn><coden>PRSTDS</coden><abstract>BACKGROUND
Tumor necrosis factor related apoptosis‐inducing ligand/Apo2 ligand (TRAIL/Apo‐2L) is a novel anticancer agent, capable of inducing apoptosis preferentially in tumor and transformed cells. TRAIL‐R1/death receptor (DR)4 and TRAIL‐R2/DR5 are members of the tumor necrosis factor (TNF) receptor family, and can be activated by the TRAIL. We examined the clinical potential of chemotherapeutic drugs and TRAIL for the treatment of prostate cancer.
METHODS
Prostate and bladder cancer cells were exposed to chemotherapeutic drugs (paclitaxel, vincristine, vinblastine, etoposide, doxorubicin, and camptothecin) and TRAIL. Cell viability was measured by sodium 3′[1‐(phenylaminocarbonyl)‐3,4‐tetrazolium]‐bis (4‐methoxy‐6‐nitro) assay; expressions of death receptors and Bcl‐2 family members were measured by Western blotting, ELISA and ribonuclease protection assay. PC‐3 tumor cells xenografted athymic nude mice were exposed to chemotherapeutic drugs and TRAIL, either alone or in combination, to measure tumor growth and survival of mice. Apoptosis was measured by annexin V–FITC/propidium iodide staining, and terminal deoxynucleotidyltransferase‐mediated nick end labeling assay. Caspase‐3 activity was measured by the Western blotting and immunohistochemistry.
RESULTS
TRAIL induced apoptosis with varying sensitivity. Chemotherapeutic drugs (paclitaxel, vincristine, vinblastine, etoposide, doxorubicin, and camptothecin) significantly augmented TRAIL‐induced apoptosis in cancer cells through up‐regulation of DR4, DR5, Bax, and Bak, and induction of caspase activation. Mitochondrial pathway enhanced the synergistic interactions between drugs and TRAIL. The sequential treatment of mice with chemotherapeutic drugs followed by TRAIL induced caspase‐3 activity, and apoptosis, inhibited angiogenesis, completely eradicated the established tumors, and enhanced survival of mice.
CONCLUSIONS
Chemotherapeutic drugs can be used to enhance the therapeutic potential of TRAIL in prostate cancer. © 2004 Wiley‐Liss, Inc.</abstract><cop>Hoboken</cop><pub>Wiley Subscription Services, Inc., A Wiley Company</pub><pmid>15389801</pmid><doi>10.1002/pros.20126</doi><tpages>22</tpages></addata></record> |
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| ispartof | The Prostate, 2005-02, Vol.62 (2), p.165-186 |
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| subjects | Androgens - metabolism Animals Antineoplastic Agents - pharmacology apoptosis Apoptosis - drug effects Apoptosis Regulatory Proteins Biological and medical sciences Caspase 3 Caspases - metabolism chemotherapy death receptors Drug Synergism Gynecology. Andrology. Obstetrics Humans In Vitro Techniques Male Medical sciences Membrane Glycoproteins - pharmacology Mice Mice, Inbred BALB C Mice, Nude Mitochondria - drug effects Mitochondria - physiology Neovascularization, Pathologic - drug therapy Neovascularization, Pathologic - mortality Nephrology. Urinary tract diseases prostate cancer Prostatic Neoplasms - drug therapy Prostatic Neoplasms - mortality Proto-Oncogene Proteins c-bcl-2 - metabolism Receptors, TNF-Related Apoptosis-Inducing Ligand Receptors, Tumor Necrosis Factor - metabolism Survival Rate TNF-Related Apoptosis-Inducing Ligand TRAIL/Apo-2L Tumor Necrosis Factor-alpha - pharmacology Tumors of the urinary system Urinary Bladder Neoplasms Urinary tract. Prostate gland |
| title | Effects of sequential treatments with chemotherapeutic drugs followed by TRAIL on prostate cancer in vitro and in vivo |
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