Synergistic Cell Death by EGCG and Ibuprofen in DU-145 Prostate Cancer Cell Line
Background: One of the green tea components epigallocatechin-3-gallate (EGCG) significantly prevented the growth of prostate cancer cells. In this study, synergistic effect of EGCG and ibuprofen (EGCG+ibuprofen) was investigated to determine their anti-proliferative and pro-apoptotic action in DU-14...
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| Veröffentlicht in: | Anticancer research 2007-11, Vol.27 (6B), p.3947-3956 |
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| creator | KIM, Myoung H CHUNG, Jaegwon |
| description | Background: One of the green tea components epigallocatechin-3-gallate (EGCG) significantly prevented the growth of prostate
cancer cells. In this study, synergistic effect of EGCG and ibuprofen (EGCG+ibuprofen) was investigated to determine their
anti-proliferative and pro-apoptotic action in DU-145 prostate cancer cells. Materials and Methods: Cell death analysis, immunoblotting,
RT-PCR analysis, and caspase activity assay were used. Results: EGCG+ibuprofen treatment resulted in 90% growth inhibition,
while ibuprofen or EGCG alone reduced cell numbers by 25% and 20%, respectively. EGCG+ibuprofen induced MAPK activation, caspase
activation and the inhibition of Bfl-1 expression, all of which were blocked by the antioxidant, N-acetyl-L-cysteine (NAC).
Moreover, addition of ceramide rescued the NAC-inhibited MAPK activation and pretreatment with the ceramide synthase inhibitor,
fumonisin B1, reduced cell death. Conclusion: Our results suggest that in DU-145 prostate cancer cells: (i) EGCG+ibuprofen
treatment has a synergistic effect on apoptosis, and (ii) oxidative stress, directly or indirectly via ceramide synthesis
mediates pro-apoptotic signaling. |
| format | Article |
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cancer cells. In this study, synergistic effect of EGCG and ibuprofen (EGCG+ibuprofen) was investigated to determine their
anti-proliferative and pro-apoptotic action in DU-145 prostate cancer cells. Materials and Methods: Cell death analysis, immunoblotting,
RT-PCR analysis, and caspase activity assay were used. Results: EGCG+ibuprofen treatment resulted in 90% growth inhibition,
while ibuprofen or EGCG alone reduced cell numbers by 25% and 20%, respectively. EGCG+ibuprofen induced MAPK activation, caspase
activation and the inhibition of Bfl-1 expression, all of which were blocked by the antioxidant, N-acetyl-L-cysteine (NAC).
Moreover, addition of ceramide rescued the NAC-inhibited MAPK activation and pretreatment with the ceramide synthase inhibitor,
fumonisin B1, reduced cell death. Conclusion: Our results suggest that in DU-145 prostate cancer cells: (i) EGCG+ibuprofen
treatment has a synergistic effect on apoptosis, and (ii) oxidative stress, directly or indirectly via ceramide synthesis
mediates pro-apoptotic signaling.</description><identifier>ISSN: 0250-7005</identifier><identifier>EISSN: 1791-7530</identifier><identifier>PMID: 18225555</identifier><language>eng</language><publisher>Attiki: International Institute of Anticancer Research</publisher><subject>Antineoplastic Combined Chemotherapy Protocols - pharmacology ; Apoptosis - drug effects ; Biological and medical sciences ; Caspases - metabolism ; Catechin - administration & dosage ; Catechin - analogs & derivatives ; Cell Line, Tumor ; Ceramides - biosynthesis ; Ceramides - pharmacology ; Drug Synergism ; Enzyme Activation - drug effects ; Humans ; Ibuprofen - administration & dosage ; Male ; Medical sciences ; Minor Histocompatibility Antigens ; Mitogen-Activated Protein Kinases - metabolism ; Nephrology. Urinary tract diseases ; Oxidative Stress ; Phosphorylation ; Prostatic Neoplasms - drug therapy ; Prostatic Neoplasms - metabolism ; Prostatic Neoplasms - pathology ; Proto-Oncogene Proteins c-bcl-2 - biosynthesis ; Tumor Suppressor Protein p53 - metabolism ; Tumors ; Tumors of the urinary system ; Urinary tract. Prostate gland</subject><ispartof>Anticancer research, 2007-11, Vol.27 (6B), p.3947-3956</ispartof><rights>2008 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=19949435$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18225555$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>KIM, Myoung H</creatorcontrib><creatorcontrib>CHUNG, Jaegwon</creatorcontrib><title>Synergistic Cell Death by EGCG and Ibuprofen in DU-145 Prostate Cancer Cell Line</title><title>Anticancer research</title><addtitle>Anticancer Res</addtitle><description>Background: One of the green tea components epigallocatechin-3-gallate (EGCG) significantly prevented the growth of prostate
cancer cells. In this study, synergistic effect of EGCG and ibuprofen (EGCG+ibuprofen) was investigated to determine their
anti-proliferative and pro-apoptotic action in DU-145 prostate cancer cells. Materials and Methods: Cell death analysis, immunoblotting,
RT-PCR analysis, and caspase activity assay were used. Results: EGCG+ibuprofen treatment resulted in 90% growth inhibition,
while ibuprofen or EGCG alone reduced cell numbers by 25% and 20%, respectively. EGCG+ibuprofen induced MAPK activation, caspase
activation and the inhibition of Bfl-1 expression, all of which were blocked by the antioxidant, N-acetyl-L-cysteine (NAC).
Moreover, addition of ceramide rescued the NAC-inhibited MAPK activation and pretreatment with the ceramide synthase inhibitor,
fumonisin B1, reduced cell death. Conclusion: Our results suggest that in DU-145 prostate cancer cells: (i) EGCG+ibuprofen
treatment has a synergistic effect on apoptosis, and (ii) oxidative stress, directly or indirectly via ceramide synthesis
mediates pro-apoptotic signaling.</description><subject>Antineoplastic Combined Chemotherapy Protocols - pharmacology</subject><subject>Apoptosis - drug effects</subject><subject>Biological and medical sciences</subject><subject>Caspases - metabolism</subject><subject>Catechin - administration & dosage</subject><subject>Catechin - analogs & derivatives</subject><subject>Cell Line, Tumor</subject><subject>Ceramides - biosynthesis</subject><subject>Ceramides - pharmacology</subject><subject>Drug Synergism</subject><subject>Enzyme Activation - drug effects</subject><subject>Humans</subject><subject>Ibuprofen - administration & dosage</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Minor Histocompatibility Antigens</subject><subject>Mitogen-Activated Protein Kinases - metabolism</subject><subject>Nephrology. Urinary tract diseases</subject><subject>Oxidative Stress</subject><subject>Phosphorylation</subject><subject>Prostatic Neoplasms - drug therapy</subject><subject>Prostatic Neoplasms - metabolism</subject><subject>Prostatic Neoplasms - pathology</subject><subject>Proto-Oncogene Proteins c-bcl-2 - biosynthesis</subject><subject>Tumor Suppressor Protein p53 - metabolism</subject><subject>Tumors</subject><subject>Tumors of the urinary system</subject><subject>Urinary tract. Prostate gland</subject><issn>0250-7005</issn><issn>1791-7530</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFj01Lw0AYhBdRbK3-BdmL3gKb_cjmPWr6YaFgQXsOm903zUqalt0U6b830opzmcszw8wVGaca0kQrwa7JmHHFEs2YGpG7GL8YyzLIxS0ZpTnnatCYrD9OHYatj723tMC2pVM0fUOrE50tigU1naPL6ngI-xo76js63SSpVHQd9rE3PdLCdBbDObryHd6Tm9q0ER8uPiGb-eyzeEtW74tl8bJKGq5Zn1hW5yCENZwpkTMEkeWVFlJphy6DWmrnKpcqsJxxADW8wjy1GmrDB5NiQh7PvYdjtUNXHoLfmXAq_64NwNMFMNGatg7DUB__OQAJUvxyz2eu8dvm2wcs48607VArShO4LrPXUoDU4gech2I4</recordid><startdate>20071101</startdate><enddate>20071101</enddate><creator>KIM, Myoung H</creator><creator>CHUNG, Jaegwon</creator><general>International Institute of Anticancer Research</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope></search><sort><creationdate>20071101</creationdate><title>Synergistic Cell Death by EGCG and Ibuprofen in DU-145 Prostate Cancer Cell Line</title><author>KIM, Myoung H ; CHUNG, Jaegwon</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-h270t-c0f8933ca205380e9368b73457ded69f47ddbd159c202995791e81c79fa21c743</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Antineoplastic Combined Chemotherapy Protocols - pharmacology</topic><topic>Apoptosis - drug effects</topic><topic>Biological and medical sciences</topic><topic>Caspases - metabolism</topic><topic>Catechin - administration & dosage</topic><topic>Catechin - analogs & derivatives</topic><topic>Cell Line, Tumor</topic><topic>Ceramides - biosynthesis</topic><topic>Ceramides - pharmacology</topic><topic>Drug Synergism</topic><topic>Enzyme Activation - drug effects</topic><topic>Humans</topic><topic>Ibuprofen - administration & dosage</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Minor Histocompatibility Antigens</topic><topic>Mitogen-Activated Protein Kinases - metabolism</topic><topic>Nephrology. Urinary tract diseases</topic><topic>Oxidative Stress</topic><topic>Phosphorylation</topic><topic>Prostatic Neoplasms - drug therapy</topic><topic>Prostatic Neoplasms - metabolism</topic><topic>Prostatic Neoplasms - pathology</topic><topic>Proto-Oncogene Proteins c-bcl-2 - biosynthesis</topic><topic>Tumor Suppressor Protein p53 - metabolism</topic><topic>Tumors</topic><topic>Tumors of the urinary system</topic><topic>Urinary tract. Prostate gland</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>KIM, Myoung H</creatorcontrib><creatorcontrib>CHUNG, Jaegwon</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><jtitle>Anticancer research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>KIM, Myoung H</au><au>CHUNG, Jaegwon</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Synergistic Cell Death by EGCG and Ibuprofen in DU-145 Prostate Cancer Cell Line</atitle><jtitle>Anticancer research</jtitle><addtitle>Anticancer Res</addtitle><date>2007-11-01</date><risdate>2007</risdate><volume>27</volume><issue>6B</issue><spage>3947</spage><epage>3956</epage><pages>3947-3956</pages><issn>0250-7005</issn><eissn>1791-7530</eissn><abstract>Background: One of the green tea components epigallocatechin-3-gallate (EGCG) significantly prevented the growth of prostate
cancer cells. In this study, synergistic effect of EGCG and ibuprofen (EGCG+ibuprofen) was investigated to determine their
anti-proliferative and pro-apoptotic action in DU-145 prostate cancer cells. Materials and Methods: Cell death analysis, immunoblotting,
RT-PCR analysis, and caspase activity assay were used. Results: EGCG+ibuprofen treatment resulted in 90% growth inhibition,
while ibuprofen or EGCG alone reduced cell numbers by 25% and 20%, respectively. EGCG+ibuprofen induced MAPK activation, caspase
activation and the inhibition of Bfl-1 expression, all of which were blocked by the antioxidant, N-acetyl-L-cysteine (NAC).
Moreover, addition of ceramide rescued the NAC-inhibited MAPK activation and pretreatment with the ceramide synthase inhibitor,
fumonisin B1, reduced cell death. Conclusion: Our results suggest that in DU-145 prostate cancer cells: (i) EGCG+ibuprofen
treatment has a synergistic effect on apoptosis, and (ii) oxidative stress, directly or indirectly via ceramide synthesis
mediates pro-apoptotic signaling.</abstract><cop>Attiki</cop><pub>International Institute of Anticancer Research</pub><pmid>18225555</pmid><tpages>10</tpages></addata></record> |
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| source | MEDLINE; EZB-FREE-00999 freely available EZB journals |
| subjects | Antineoplastic Combined Chemotherapy Protocols - pharmacology Apoptosis - drug effects Biological and medical sciences Caspases - metabolism Catechin - administration & dosage Catechin - analogs & derivatives Cell Line, Tumor Ceramides - biosynthesis Ceramides - pharmacology Drug Synergism Enzyme Activation - drug effects Humans Ibuprofen - administration & dosage Male Medical sciences Minor Histocompatibility Antigens Mitogen-Activated Protein Kinases - metabolism Nephrology. Urinary tract diseases Oxidative Stress Phosphorylation Prostatic Neoplasms - drug therapy Prostatic Neoplasms - metabolism Prostatic Neoplasms - pathology Proto-Oncogene Proteins c-bcl-2 - biosynthesis Tumor Suppressor Protein p53 - metabolism Tumors Tumors of the urinary system Urinary tract. Prostate gland |
| title | Synergistic Cell Death by EGCG and Ibuprofen in DU-145 Prostate Cancer Cell Line |
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