Sensitization of colon cancer cell lines to butyrate-mediated proliferation inhibition by combined application of indomethacin and nordihydroguaiaretic acid
The aim of the study was to investigate the effects of nonsteroidal anti-inflammatory drugs (NSAIDs) on histone deacetylase-mediated proliferation inhibition. In the colon cancer cell line HT29 butyrate-mediated proliferation inhibition was enhanced by the additional presence of indomethacin (IM) an...
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| Veröffentlicht in: | Cancer detection and prevention 2005-01, Vol.29 (3), p.276-285 |
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| creator | Galfi, Peter Neogrady, Zsuzsa Amberger, Albert Margreiter, Raimund Csordas, Adam |
| description | The aim of the study was to investigate the effects of nonsteroidal anti-inflammatory drugs (NSAIDs) on histone deacetylase-mediated proliferation inhibition. In the colon cancer cell line HT29 butyrate-mediated proliferation inhibition was enhanced by the additional presence of indomethacin (IM) and/or nordihydroguaiaretic acid (NDGA). Sensitisation to butyrate-mediated proliferation inhibition was abolished by the general caspase inhibitor Z-VAD-fmk, however, only IM-induced cell detachment was prevented by the caspase inhibitor but not that induced by NDGA or NDGA plus IM. In contrast to the parental cell line HT29, in the methotrexate-resistant sub-lines HT29-12 and HT29-21, IM counteracted butyrate-mediated proliferation inhibition, which was abrogated by NDGA. In all the investigated cell lines, proliferation inhibition was most effectively achieved under the combined application of butyrate with IM and NDGA, suggesting that inhibition of both cyclooxygenase (COX) and lipoxygenase (LOX) isoenzymes is needed for proliferation inhibition by NSAIDs in tumour cells. |
| doi_str_mv | 10.1016/j.cdp.2004.12.001 |
| format | Article |
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In the colon cancer cell line HT29 butyrate-mediated proliferation inhibition was enhanced by the additional presence of indomethacin (IM) and/or nordihydroguaiaretic acid (NDGA). Sensitisation to butyrate-mediated proliferation inhibition was abolished by the general caspase inhibitor Z-VAD-fmk, however, only IM-induced cell detachment was prevented by the caspase inhibitor but not that induced by NDGA or NDGA plus IM. In contrast to the parental cell line HT29, in the methotrexate-resistant sub-lines HT29-12 and HT29-21, IM counteracted butyrate-mediated proliferation inhibition, which was abrogated by NDGA. In all the investigated cell lines, proliferation inhibition was most effectively achieved under the combined application of butyrate with IM and NDGA, suggesting that inhibition of both cyclooxygenase (COX) and lipoxygenase (LOX) isoenzymes is needed for proliferation inhibition by NSAIDs in tumour cells.</description><identifier>ISSN: 0361-090X</identifier><identifier>ISSN: 1877-7821</identifier><identifier>EISSN: 1873-443X</identifier><identifier>EISSN: 1877-783X</identifier><identifier>DOI: 10.1016/j.cdp.2004.12.001</identifier><identifier>PMID: 15936596</identifier><identifier>CODEN: CDPRD4</identifier><language>eng</language><publisher>England: Elsevier Ltd</publisher><subject>Anti-Inflammatory Agents, Non-Steroidal - pharmacology ; Antioxidants - pharmacology ; Apoptosis ; Butyrate ; Butyrates - pharmacology ; Cancer ; Cancer therapies ; Cell growth ; Cell Line, Tumor ; Cell Proliferation - drug effects ; Colon ; Colon cancer cell lines ; Colonic Neoplasms - pathology ; Colorectal cancer ; Cyclooxygenase Inhibitors - pharmacology ; Cyclooxygenases ; Disease prevention ; Drug Interactions ; Drug Resistance, Neoplasm ; Enzymes ; Epidemiology ; Genotype & phenotype ; Humans ; Indomethacin ; Indomethacin - pharmacology ; Isoenzymes ; Lipoxygenase Inhibitors - pharmacology ; Lipoxygenases ; Masoprocol - pharmacology ; NDGA ; Nonsteroidal anti-inflammatory drugs ; NSAIDs ; Proliferation inhibition ; Rodents ; Studies ; Veterinary medicine</subject><ispartof>Cancer detection and prevention, 2005-01, Vol.29 (3), p.276-285</ispartof><rights>2004 International Society for Preventive Oncology</rights><rights>Copyright Elsevier Limited 2005</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c379t-c647b5b83ae362d289d5a5ecf877aa074c4e84635582cc15434aa496ab05a59b3</citedby><cites>FETCH-LOGICAL-c379t-c647b5b83ae362d289d5a5ecf877aa074c4e84635582cc15434aa496ab05a59b3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.proquest.com/docview/1418661006?pq-origsite=primo$$EHTML$$P50$$Gproquest$$H</linktohtml><link.rule.ids>314,780,784,27924,27925,64385,64389,72469</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15936596$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Galfi, Peter</creatorcontrib><creatorcontrib>Neogrady, Zsuzsa</creatorcontrib><creatorcontrib>Amberger, Albert</creatorcontrib><creatorcontrib>Margreiter, Raimund</creatorcontrib><creatorcontrib>Csordas, Adam</creatorcontrib><title>Sensitization of colon cancer cell lines to butyrate-mediated proliferation inhibition by combined application of indomethacin and nordihydroguaiaretic acid</title><title>Cancer detection and prevention</title><addtitle>Cancer Detect Prev</addtitle><description>The aim of the study was to investigate the effects of nonsteroidal anti-inflammatory drugs (NSAIDs) on histone deacetylase-mediated proliferation inhibition. In the colon cancer cell line HT29 butyrate-mediated proliferation inhibition was enhanced by the additional presence of indomethacin (IM) and/or nordihydroguaiaretic acid (NDGA). Sensitisation to butyrate-mediated proliferation inhibition was abolished by the general caspase inhibitor Z-VAD-fmk, however, only IM-induced cell detachment was prevented by the caspase inhibitor but not that induced by NDGA or NDGA plus IM. In contrast to the parental cell line HT29, in the methotrexate-resistant sub-lines HT29-12 and HT29-21, IM counteracted butyrate-mediated proliferation inhibition, which was abrogated by NDGA. In all the investigated cell lines, proliferation inhibition was most effectively achieved under the combined application of butyrate with IM and NDGA, suggesting that inhibition of both cyclooxygenase (COX) and lipoxygenase (LOX) isoenzymes is needed for proliferation inhibition by NSAIDs in tumour cells.</description><subject>Anti-Inflammatory Agents, Non-Steroidal - pharmacology</subject><subject>Antioxidants - pharmacology</subject><subject>Apoptosis</subject><subject>Butyrate</subject><subject>Butyrates - pharmacology</subject><subject>Cancer</subject><subject>Cancer therapies</subject><subject>Cell growth</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation - drug effects</subject><subject>Colon</subject><subject>Colon cancer cell lines</subject><subject>Colonic Neoplasms - pathology</subject><subject>Colorectal cancer</subject><subject>Cyclooxygenase Inhibitors - pharmacology</subject><subject>Cyclooxygenases</subject><subject>Disease prevention</subject><subject>Drug Interactions</subject><subject>Drug Resistance, Neoplasm</subject><subject>Enzymes</subject><subject>Epidemiology</subject><subject>Genotype & phenotype</subject><subject>Humans</subject><subject>Indomethacin</subject><subject>Indomethacin - pharmacology</subject><subject>Isoenzymes</subject><subject>Lipoxygenase Inhibitors - pharmacology</subject><subject>Lipoxygenases</subject><subject>Masoprocol - pharmacology</subject><subject>NDGA</subject><subject>Nonsteroidal anti-inflammatory drugs</subject><subject>NSAIDs</subject><subject>Proliferation inhibition</subject><subject>Rodents</subject><subject>Studies</subject><subject>Veterinary medicine</subject><issn>0361-090X</issn><issn>1877-7821</issn><issn>1873-443X</issn><issn>1877-783X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</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>eNp9UU2LFDEUDKK44-oP8CIBz90mnXS6G0-y-AULHlTYW8jHa-cNPUmbpIXxt_hjzTqD3jzVg1dVj1dFyHPOWs64enVonV_bjjHZ8q5ljD8gOz4OopFS3D0kOyYUb9jE7q7Ik5wPlaAmoR6TK95X7Ce1I78-Q8hY8KcpGAONM3VxqYMzwUGiDpaFLhgg0xKp3copmQLNETxW9HRNccEZ0lmNYY8W_4z2VI2Otio9Neu6oPt7AIOPRyh74zBQEzwNMXncn3yK3zaDJkFBR-vWPyWPZrNkeHbBa_L13dsvNx-a20_vP968uW2cGKbSOCUH29tRGBCq8904-d704OZxGIxhg3QSRqlE34-dc7yXQhojJ2Usq7zJimvy8uxb3_m-QS76ELcU6knNJR-V4oypyuJnlksx5wSzXhMeTTppzvR9H_qgax_6vg_NO13jrpoXF-fN1tD-KS4FVMLrMwHqfz8Qks4OoWbvMYEr2kf8j_1v8YyfWg</recordid><startdate>20050101</startdate><enddate>20050101</enddate><creator>Galfi, Peter</creator><creator>Neogrady, Zsuzsa</creator><creator>Amberger, Albert</creator><creator>Margreiter, Raimund</creator><creator>Csordas, Adam</creator><general>Elsevier Ltd</general><general>Elsevier Limited</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>3V.</scope><scope>7RV</scope><scope>7TO</scope><scope>7X7</scope><scope>7XB</scope><scope>88C</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>K9.</scope><scope>KB0</scope><scope>M0S</scope><scope>M0T</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope></search><sort><creationdate>20050101</creationdate><title>Sensitization of colon cancer cell lines to butyrate-mediated proliferation inhibition by combined application of indomethacin and nordihydroguaiaretic acid</title><author>Galfi, Peter ; Neogrady, Zsuzsa ; Amberger, Albert ; Margreiter, Raimund ; Csordas, Adam</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c379t-c647b5b83ae362d289d5a5ecf877aa074c4e84635582cc15434aa496ab05a59b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Anti-Inflammatory Agents, Non-Steroidal - pharmacology</topic><topic>Antioxidants - pharmacology</topic><topic>Apoptosis</topic><topic>Butyrate</topic><topic>Butyrates - pharmacology</topic><topic>Cancer</topic><topic>Cancer therapies</topic><topic>Cell growth</topic><topic>Cell Line, Tumor</topic><topic>Cell Proliferation - drug effects</topic><topic>Colon</topic><topic>Colon cancer cell lines</topic><topic>Colonic Neoplasms - pathology</topic><topic>Colorectal cancer</topic><topic>Cyclooxygenase Inhibitors - pharmacology</topic><topic>Cyclooxygenases</topic><topic>Disease prevention</topic><topic>Drug Interactions</topic><topic>Drug Resistance, Neoplasm</topic><topic>Enzymes</topic><topic>Epidemiology</topic><topic>Genotype & phenotype</topic><topic>Humans</topic><topic>Indomethacin</topic><topic>Indomethacin - pharmacology</topic><topic>Isoenzymes</topic><topic>Lipoxygenase Inhibitors - pharmacology</topic><topic>Lipoxygenases</topic><topic>Masoprocol - pharmacology</topic><topic>NDGA</topic><topic>Nonsteroidal anti-inflammatory drugs</topic><topic>NSAIDs</topic><topic>Proliferation inhibition</topic><topic>Rodents</topic><topic>Studies</topic><topic>Veterinary medicine</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Galfi, Peter</creatorcontrib><creatorcontrib>Neogrady, Zsuzsa</creatorcontrib><creatorcontrib>Amberger, Albert</creatorcontrib><creatorcontrib>Margreiter, Raimund</creatorcontrib><creatorcontrib>Csordas, Adam</creatorcontrib><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>Nursing & Allied Health Database</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Healthcare Administration Database (Alumni)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</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>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</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>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Healthcare Administration Database</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Research Library (Corporate)</collection><collection>Nursing & Allied Health Premium</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><jtitle>Cancer detection and prevention</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Galfi, Peter</au><au>Neogrady, Zsuzsa</au><au>Amberger, Albert</au><au>Margreiter, Raimund</au><au>Csordas, Adam</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Sensitization of colon cancer cell lines to butyrate-mediated proliferation inhibition by combined application of indomethacin and nordihydroguaiaretic acid</atitle><jtitle>Cancer detection and prevention</jtitle><addtitle>Cancer Detect Prev</addtitle><date>2005-01-01</date><risdate>2005</risdate><volume>29</volume><issue>3</issue><spage>276</spage><epage>285</epage><pages>276-285</pages><issn>0361-090X</issn><issn>1877-7821</issn><eissn>1873-443X</eissn><eissn>1877-783X</eissn><coden>CDPRD4</coden><abstract>The aim of the study was to investigate the effects of nonsteroidal anti-inflammatory drugs (NSAIDs) on histone deacetylase-mediated proliferation inhibition. In the colon cancer cell line HT29 butyrate-mediated proliferation inhibition was enhanced by the additional presence of indomethacin (IM) and/or nordihydroguaiaretic acid (NDGA). Sensitisation to butyrate-mediated proliferation inhibition was abolished by the general caspase inhibitor Z-VAD-fmk, however, only IM-induced cell detachment was prevented by the caspase inhibitor but not that induced by NDGA or NDGA plus IM. In contrast to the parental cell line HT29, in the methotrexate-resistant sub-lines HT29-12 and HT29-21, IM counteracted butyrate-mediated proliferation inhibition, which was abrogated by NDGA. In all the investigated cell lines, proliferation inhibition was most effectively achieved under the combined application of butyrate with IM and NDGA, suggesting that inhibition of both cyclooxygenase (COX) and lipoxygenase (LOX) isoenzymes is needed for proliferation inhibition by NSAIDs in tumour cells.</abstract><cop>England</cop><pub>Elsevier Ltd</pub><pmid>15936596</pmid><doi>10.1016/j.cdp.2004.12.001</doi><tpages>10</tpages></addata></record> |
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| subjects | Anti-Inflammatory Agents, Non-Steroidal - pharmacology Antioxidants - pharmacology Apoptosis Butyrate Butyrates - pharmacology Cancer Cancer therapies Cell growth Cell Line, Tumor Cell Proliferation - drug effects Colon Colon cancer cell lines Colonic Neoplasms - pathology Colorectal cancer Cyclooxygenase Inhibitors - pharmacology Cyclooxygenases Disease prevention Drug Interactions Drug Resistance, Neoplasm Enzymes Epidemiology Genotype & phenotype Humans Indomethacin Indomethacin - pharmacology Isoenzymes Lipoxygenase Inhibitors - pharmacology Lipoxygenases Masoprocol - pharmacology NDGA Nonsteroidal anti-inflammatory drugs NSAIDs Proliferation inhibition Rodents Studies Veterinary medicine |
| title | Sensitization of colon cancer cell lines to butyrate-mediated proliferation inhibition by combined application of indomethacin and nordihydroguaiaretic acid |
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