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Tumor Necrosis Factor-related Apoptosis-inducing Ligand (TRAIL)-Troglitazone-induced Apoptosis in Prostate Cancer Cells Involve AMP-activated Protein Kinase
Prostate cancer (PCa) is one of the most frequently diagnosed cancers in men with limited treatment options for the hormone-resistant forms. Development of novel therapeutic options is critically needed to target advanced forms. Here we demonstrate that combinatorial treatment with the thiazolidined...
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| Published in: | The Journal of biological chemistry 2015-09, Vol.290 (36), p.21865-21875 |
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| creator | Santha, Sreevidya Viswakarma, Navin Das, Subhasis Rana, Ajay Rana, Basabi |
| description | Prostate cancer (PCa) is one of the most frequently diagnosed cancers in men with limited treatment options for the hormone-resistant forms. Development of novel therapeutic options is critically needed to target advanced forms. Here we demonstrate that combinatorial treatment with the thiazolidinedione troglitazone (TZD) and TNF-related apoptosis-inducing ligand (TRAIL) can induce significant apoptosis in various PCa cells independent of androgen receptor status. Because TZD is known to activate AMP-activated protein kinase (AMPK), we determined whether AMPK is a molecular target mediating this apoptotic cascade by utilizing PCa cell lines stably overexpressing AMPKα1 dominant negative (C4-2-DN) or empty vector (C4-2-EV). Our results indicated a significantly higher degree of apoptosis with TRAIL-TZD combination in C4-2-EV cells compared with C4-2-DN cells. Similarly, results from a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay showed a larger reduction of viability of C4-2-EV cells compared with C4-2-DN cells when treated with TRAIL-TZD, thus suggesting that C4-2-DN cells were more apoptosis-resistant. Additionally, siRNA-mediated knockdown of endogenous AMPKα1 expression showed a reduction of TRAIL-TZD-induced apoptosis, further confirming the participation of AMPK in mediating this apoptosis. Apoptosis induction by this combinatorial treatment was also associated with a cleavage of β-catenin that was inhibited in both C4-2-DN cells and those cells in which AMPKα1 was knocked down. In addition, time course studies showed an increase in pACCS79 (AMPK target) levels coinciding with the time of apoptosis. These studies indicate the involvement of AMPK in TRAIL-TZD-mediated apoptosis and β-catenin cleavage and suggest the possibility of utilizing AMPK as a therapeutic target in apoptosis-resistant prostate cancer.
Background: Combination of TRAIL with PPARγ ligands has been shown to ameliorate TRAIL resistance, but the mechanism involved is still unknown.
Results: Inhibition of AMPK activity antagonizes TRAIL and troglitazone combination-induced apoptosis and attenuates caspase cleavage in prostate cancer cells.
Conclusion: AMPK is involved in mediating TRAIL-troglitazone-induced apoptosis.
Significance: Targeting AMPK by TRAIL and troglitazone combination might be an effective means of sensitizing apoptosis-resistant prostate cancer cells. |
| doi_str_mv | 10.1074/jbc.M115.663526 |
| format | article |
| fullrecord | <record><control><sourceid>elsevier_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_4571942</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>S0021925820448501</els_id><sourcerecordid>S0021925820448501</sourcerecordid><originalsourceid>FETCH-LOGICAL-c443t-4dabed804f1f3e4e7b43b80828f3745e33edd4323373d5d2a27dcff61fcbf0673</originalsourceid><addsrcrecordid>eNp1kUtvEzEUhS1ERdPCmh3yEhaT-jWvDVIUtSUihQoFiZ3lsa-Dq4kdeZyR6G_pj8VhoGoXeOPFPec7uvcg9JaSOSW1uLjr9PyG0nJeVbxk1Qs0o6ThBS_pj5doRgijRcvK5hSdDcMdyU-09BU6ZRVtm0qQGXrYHHYh4i-gYxjcgK-UTiEWEXqVwODFPuzTcVA4bw7a-S1eu63yBr_ffFus1h-KTQzb3iV1HzxMoqc27Dy-zeSUaXipvIaIl9D3A175MfQj4MXNbZEz3fgnL2sTZM9n59UAr9GJVf0Ab_7-5-j71eVm-alYf71eLRfrQgvBUyGM6sA0RFhqOQioO8G7hjSssbwWJXAOxgjOOK-5KQ1TrDba2opa3VlS1fwcfZy4-0O3A6PBp6h6uY9up-IvGZSTzyfe_ZTbMEpR1rQVLAMuJsDxikME--ilRB6LkrkoeSxKTkVlx7unkY_6f81kQTsJIC8-Oohy0A7yAY2LoJM0wf0X_htZnqb0</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype></control><display><type>article</type><title>Tumor Necrosis Factor-related Apoptosis-inducing Ligand (TRAIL)-Troglitazone-induced Apoptosis in Prostate Cancer Cells Involve AMP-activated Protein Kinase</title><source>BACON - Elsevier - GLOBAL_SCIENCEDIRECT-OPENACCESS</source><source>Open Access: PubMed Central</source><creator>Santha, Sreevidya ; Viswakarma, Navin ; Das, Subhasis ; Rana, Ajay ; Rana, Basabi</creator><creatorcontrib>Santha, Sreevidya ; Viswakarma, Navin ; Das, Subhasis ; Rana, Ajay ; Rana, Basabi</creatorcontrib><description>Prostate cancer (PCa) is one of the most frequently diagnosed cancers in men with limited treatment options for the hormone-resistant forms. Development of novel therapeutic options is critically needed to target advanced forms. Here we demonstrate that combinatorial treatment with the thiazolidinedione troglitazone (TZD) and TNF-related apoptosis-inducing ligand (TRAIL) can induce significant apoptosis in various PCa cells independent of androgen receptor status. Because TZD is known to activate AMP-activated protein kinase (AMPK), we determined whether AMPK is a molecular target mediating this apoptotic cascade by utilizing PCa cell lines stably overexpressing AMPKα1 dominant negative (C4-2-DN) or empty vector (C4-2-EV). Our results indicated a significantly higher degree of apoptosis with TRAIL-TZD combination in C4-2-EV cells compared with C4-2-DN cells. Similarly, results from a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay showed a larger reduction of viability of C4-2-EV cells compared with C4-2-DN cells when treated with TRAIL-TZD, thus suggesting that C4-2-DN cells were more apoptosis-resistant. Additionally, siRNA-mediated knockdown of endogenous AMPKα1 expression showed a reduction of TRAIL-TZD-induced apoptosis, further confirming the participation of AMPK in mediating this apoptosis. Apoptosis induction by this combinatorial treatment was also associated with a cleavage of β-catenin that was inhibited in both C4-2-DN cells and those cells in which AMPKα1 was knocked down. In addition, time course studies showed an increase in pACCS79 (AMPK target) levels coinciding with the time of apoptosis. These studies indicate the involvement of AMPK in TRAIL-TZD-mediated apoptosis and β-catenin cleavage and suggest the possibility of utilizing AMPK as a therapeutic target in apoptosis-resistant prostate cancer.
Background: Combination of TRAIL with PPARγ ligands has been shown to ameliorate TRAIL resistance, but the mechanism involved is still unknown.
Results: Inhibition of AMPK activity antagonizes TRAIL and troglitazone combination-induced apoptosis and attenuates caspase cleavage in prostate cancer cells.
Conclusion: AMPK is involved in mediating TRAIL-troglitazone-induced apoptosis.
Significance: Targeting AMPK by TRAIL and troglitazone combination might be an effective means of sensitizing apoptosis-resistant prostate cancer cells.</description><identifier>ISSN: 0021-9258</identifier><identifier>EISSN: 1083-351X</identifier><identifier>DOI: 10.1074/jbc.M115.663526</identifier><identifier>PMID: 26198640</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>AMP-activated kinase (AMPK) ; AMP-Activated Protein Kinases - genetics ; AMP-Activated Protein Kinases - metabolism ; apoptosis ; Apoptosis - drug effects ; beta Catenin - metabolism ; beta-catenin (B-catenin) ; Blotting, Western ; Cell Biology ; Cell Line, Tumor ; Cell Survival - drug effects ; Cell Survival - genetics ; Chromans - pharmacology ; Dose-Response Relationship, Drug ; Drug Synergism ; Humans ; Male ; PPAR gamma - agonists ; PPAR gamma - genetics ; PPAR gamma - metabolism ; prostate cancer ; Prostatic Neoplasms - enzymology ; Prostatic Neoplasms - genetics ; Prostatic Neoplasms - pathology ; RNA Interference ; Signal Transduction - drug effects ; Signal Transduction - genetics ; Thiazolidinediones - pharmacology ; Time Factors ; TNF-Related Apoptosis-Inducing Ligand - pharmacology ; TRAIL ; Troglitazone</subject><ispartof>The Journal of biological chemistry, 2015-09, Vol.290 (36), p.21865-21875</ispartof><rights>2015 © 2015 ASBMB. Currently published by Elsevier Inc; originally published by American Society for Biochemistry and Molecular Biology.</rights><rights>2015 by The American Society for Biochemistry and Molecular Biology, Inc.</rights><rights>2015 by The American Society for Biochemistry and Molecular Biology, Inc. 2015 The American Society for Biochemistry and Molecular Biology, Inc.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c443t-4dabed804f1f3e4e7b43b80828f3745e33edd4323373d5d2a27dcff61fcbf0673</citedby><cites>FETCH-LOGICAL-c443t-4dabed804f1f3e4e7b43b80828f3745e33edd4323373d5d2a27dcff61fcbf0673</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/PMC4571942/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4571942/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,315,733,786,790,891,27957,27958,53827,53829</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26198640$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Santha, Sreevidya</creatorcontrib><creatorcontrib>Viswakarma, Navin</creatorcontrib><creatorcontrib>Das, Subhasis</creatorcontrib><creatorcontrib>Rana, Ajay</creatorcontrib><creatorcontrib>Rana, Basabi</creatorcontrib><title>Tumor Necrosis Factor-related Apoptosis-inducing Ligand (TRAIL)-Troglitazone-induced Apoptosis in Prostate Cancer Cells Involve AMP-activated Protein Kinase</title><title>The Journal of biological chemistry</title><addtitle>J Biol Chem</addtitle><description>Prostate cancer (PCa) is one of the most frequently diagnosed cancers in men with limited treatment options for the hormone-resistant forms. Development of novel therapeutic options is critically needed to target advanced forms. Here we demonstrate that combinatorial treatment with the thiazolidinedione troglitazone (TZD) and TNF-related apoptosis-inducing ligand (TRAIL) can induce significant apoptosis in various PCa cells independent of androgen receptor status. Because TZD is known to activate AMP-activated protein kinase (AMPK), we determined whether AMPK is a molecular target mediating this apoptotic cascade by utilizing PCa cell lines stably overexpressing AMPKα1 dominant negative (C4-2-DN) or empty vector (C4-2-EV). Our results indicated a significantly higher degree of apoptosis with TRAIL-TZD combination in C4-2-EV cells compared with C4-2-DN cells. Similarly, results from a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay showed a larger reduction of viability of C4-2-EV cells compared with C4-2-DN cells when treated with TRAIL-TZD, thus suggesting that C4-2-DN cells were more apoptosis-resistant. Additionally, siRNA-mediated knockdown of endogenous AMPKα1 expression showed a reduction of TRAIL-TZD-induced apoptosis, further confirming the participation of AMPK in mediating this apoptosis. Apoptosis induction by this combinatorial treatment was also associated with a cleavage of β-catenin that was inhibited in both C4-2-DN cells and those cells in which AMPKα1 was knocked down. In addition, time course studies showed an increase in pACCS79 (AMPK target) levels coinciding with the time of apoptosis. These studies indicate the involvement of AMPK in TRAIL-TZD-mediated apoptosis and β-catenin cleavage and suggest the possibility of utilizing AMPK as a therapeutic target in apoptosis-resistant prostate cancer.
Background: Combination of TRAIL with PPARγ ligands has been shown to ameliorate TRAIL resistance, but the mechanism involved is still unknown.
Results: Inhibition of AMPK activity antagonizes TRAIL and troglitazone combination-induced apoptosis and attenuates caspase cleavage in prostate cancer cells.
Conclusion: AMPK is involved in mediating TRAIL-troglitazone-induced apoptosis.
Significance: Targeting AMPK by TRAIL and troglitazone combination might be an effective means of sensitizing apoptosis-resistant prostate cancer cells.</description><subject>AMP-activated kinase (AMPK)</subject><subject>AMP-Activated Protein Kinases - genetics</subject><subject>AMP-Activated Protein Kinases - metabolism</subject><subject>apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>beta Catenin - metabolism</subject><subject>beta-catenin (B-catenin)</subject><subject>Blotting, Western</subject><subject>Cell Biology</subject><subject>Cell Line, Tumor</subject><subject>Cell Survival - drug effects</subject><subject>Cell Survival - genetics</subject><subject>Chromans - pharmacology</subject><subject>Dose-Response Relationship, Drug</subject><subject>Drug Synergism</subject><subject>Humans</subject><subject>Male</subject><subject>PPAR gamma - agonists</subject><subject>PPAR gamma - genetics</subject><subject>PPAR gamma - metabolism</subject><subject>prostate cancer</subject><subject>Prostatic Neoplasms - enzymology</subject><subject>Prostatic Neoplasms - genetics</subject><subject>Prostatic Neoplasms - pathology</subject><subject>RNA Interference</subject><subject>Signal Transduction - drug effects</subject><subject>Signal Transduction - genetics</subject><subject>Thiazolidinediones - pharmacology</subject><subject>Time Factors</subject><subject>TNF-Related Apoptosis-Inducing Ligand - pharmacology</subject><subject>TRAIL</subject><subject>Troglitazone</subject><issn>0021-9258</issn><issn>1083-351X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><recordid>eNp1kUtvEzEUhS1ERdPCmh3yEhaT-jWvDVIUtSUihQoFiZ3lsa-Dq4kdeZyR6G_pj8VhoGoXeOPFPec7uvcg9JaSOSW1uLjr9PyG0nJeVbxk1Qs0o6ThBS_pj5doRgijRcvK5hSdDcMdyU-09BU6ZRVtm0qQGXrYHHYh4i-gYxjcgK-UTiEWEXqVwODFPuzTcVA4bw7a-S1eu63yBr_ffFus1h-KTQzb3iV1HzxMoqc27Dy-zeSUaXipvIaIl9D3A175MfQj4MXNbZEz3fgnL2sTZM9n59UAr9GJVf0Ab_7-5-j71eVm-alYf71eLRfrQgvBUyGM6sA0RFhqOQioO8G7hjSssbwWJXAOxgjOOK-5KQ1TrDba2opa3VlS1fwcfZy4-0O3A6PBp6h6uY9up-IvGZSTzyfe_ZTbMEpR1rQVLAMuJsDxikME--ilRB6LkrkoeSxKTkVlx7unkY_6f81kQTsJIC8-Oohy0A7yAY2LoJM0wf0X_htZnqb0</recordid><startdate>20150904</startdate><enddate>20150904</enddate><creator>Santha, Sreevidya</creator><creator>Viswakarma, Navin</creator><creator>Das, Subhasis</creator><creator>Rana, Ajay</creator><creator>Rana, Basabi</creator><general>Elsevier Inc</general><general>American Society for Biochemistry and Molecular Biology</general><scope>6I.</scope><scope>AAFTH</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>5PM</scope></search><sort><creationdate>20150904</creationdate><title>Tumor Necrosis Factor-related Apoptosis-inducing Ligand (TRAIL)-Troglitazone-induced Apoptosis in Prostate Cancer Cells Involve AMP-activated Protein Kinase</title><author>Santha, Sreevidya ; Viswakarma, Navin ; Das, Subhasis ; Rana, Ajay ; Rana, Basabi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c443t-4dabed804f1f3e4e7b43b80828f3745e33edd4323373d5d2a27dcff61fcbf0673</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>AMP-activated kinase (AMPK)</topic><topic>AMP-Activated Protein Kinases - genetics</topic><topic>AMP-Activated Protein Kinases - metabolism</topic><topic>apoptosis</topic><topic>Apoptosis - drug effects</topic><topic>beta Catenin - metabolism</topic><topic>beta-catenin (B-catenin)</topic><topic>Blotting, Western</topic><topic>Cell Biology</topic><topic>Cell Line, Tumor</topic><topic>Cell Survival - drug effects</topic><topic>Cell Survival - genetics</topic><topic>Chromans - pharmacology</topic><topic>Dose-Response Relationship, Drug</topic><topic>Drug Synergism</topic><topic>Humans</topic><topic>Male</topic><topic>PPAR gamma - agonists</topic><topic>PPAR gamma - genetics</topic><topic>PPAR gamma - metabolism</topic><topic>prostate cancer</topic><topic>Prostatic Neoplasms - enzymology</topic><topic>Prostatic Neoplasms - genetics</topic><topic>Prostatic Neoplasms - pathology</topic><topic>RNA Interference</topic><topic>Signal Transduction - drug effects</topic><topic>Signal Transduction - genetics</topic><topic>Thiazolidinediones - pharmacology</topic><topic>Time Factors</topic><topic>TNF-Related Apoptosis-Inducing Ligand - pharmacology</topic><topic>TRAIL</topic><topic>Troglitazone</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Santha, Sreevidya</creatorcontrib><creatorcontrib>Viswakarma, Navin</creatorcontrib><creatorcontrib>Das, Subhasis</creatorcontrib><creatorcontrib>Rana, Ajay</creatorcontrib><creatorcontrib>Rana, Basabi</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>The Journal of biological chemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Santha, Sreevidya</au><au>Viswakarma, Navin</au><au>Das, Subhasis</au><au>Rana, Ajay</au><au>Rana, Basabi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Tumor Necrosis Factor-related Apoptosis-inducing Ligand (TRAIL)-Troglitazone-induced Apoptosis in Prostate Cancer Cells Involve AMP-activated Protein Kinase</atitle><jtitle>The Journal of biological chemistry</jtitle><addtitle>J Biol Chem</addtitle><date>2015-09-04</date><risdate>2015</risdate><volume>290</volume><issue>36</issue><spage>21865</spage><epage>21875</epage><pages>21865-21875</pages><issn>0021-9258</issn><eissn>1083-351X</eissn><abstract>Prostate cancer (PCa) is one of the most frequently diagnosed cancers in men with limited treatment options for the hormone-resistant forms. Development of novel therapeutic options is critically needed to target advanced forms. Here we demonstrate that combinatorial treatment with the thiazolidinedione troglitazone (TZD) and TNF-related apoptosis-inducing ligand (TRAIL) can induce significant apoptosis in various PCa cells independent of androgen receptor status. Because TZD is known to activate AMP-activated protein kinase (AMPK), we determined whether AMPK is a molecular target mediating this apoptotic cascade by utilizing PCa cell lines stably overexpressing AMPKα1 dominant negative (C4-2-DN) or empty vector (C4-2-EV). Our results indicated a significantly higher degree of apoptosis with TRAIL-TZD combination in C4-2-EV cells compared with C4-2-DN cells. Similarly, results from a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay showed a larger reduction of viability of C4-2-EV cells compared with C4-2-DN cells when treated with TRAIL-TZD, thus suggesting that C4-2-DN cells were more apoptosis-resistant. Additionally, siRNA-mediated knockdown of endogenous AMPKα1 expression showed a reduction of TRAIL-TZD-induced apoptosis, further confirming the participation of AMPK in mediating this apoptosis. Apoptosis induction by this combinatorial treatment was also associated with a cleavage of β-catenin that was inhibited in both C4-2-DN cells and those cells in which AMPKα1 was knocked down. In addition, time course studies showed an increase in pACCS79 (AMPK target) levels coinciding with the time of apoptosis. These studies indicate the involvement of AMPK in TRAIL-TZD-mediated apoptosis and β-catenin cleavage and suggest the possibility of utilizing AMPK as a therapeutic target in apoptosis-resistant prostate cancer.
Background: Combination of TRAIL with PPARγ ligands has been shown to ameliorate TRAIL resistance, but the mechanism involved is still unknown.
Results: Inhibition of AMPK activity antagonizes TRAIL and troglitazone combination-induced apoptosis and attenuates caspase cleavage in prostate cancer cells.
Conclusion: AMPK is involved in mediating TRAIL-troglitazone-induced apoptosis.
Significance: Targeting AMPK by TRAIL and troglitazone combination might be an effective means of sensitizing apoptosis-resistant prostate cancer cells.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>26198640</pmid><doi>10.1074/jbc.M115.663526</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | AMP-activated kinase (AMPK) AMP-Activated Protein Kinases - genetics AMP-Activated Protein Kinases - metabolism apoptosis Apoptosis - drug effects beta Catenin - metabolism beta-catenin (B-catenin) Blotting, Western Cell Biology Cell Line, Tumor Cell Survival - drug effects Cell Survival - genetics Chromans - pharmacology Dose-Response Relationship, Drug Drug Synergism Humans Male PPAR gamma - agonists PPAR gamma - genetics PPAR gamma - metabolism prostate cancer Prostatic Neoplasms - enzymology Prostatic Neoplasms - genetics Prostatic Neoplasms - pathology RNA Interference Signal Transduction - drug effects Signal Transduction - genetics Thiazolidinediones - pharmacology Time Factors TNF-Related Apoptosis-Inducing Ligand - pharmacology TRAIL Troglitazone |
| title | Tumor Necrosis Factor-related Apoptosis-inducing Ligand (TRAIL)-Troglitazone-induced Apoptosis in Prostate Cancer Cells Involve AMP-activated Protein Kinase |
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