Opposite effects of antimicrotubule agents on c- myc oncogene expression depending on the cell lines used
We investigated the expression of c- myc in HT29-D4, HBL100 and Caco-2 cells treated with microtubule stabilising (paclitaxel) or depolymerising agents (vinblastine, nocodazole). After induction by epidermal growth factor (EGF), c- myc expression decreased in HT29-D4 cells treated with all the antim...
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| Veröffentlicht in: | European journal of cancer (1990) 2000-05, Vol.36 (8), p.1043-1049 |
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| container_title | European journal of cancer (1990) |
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| creator | Bourgarel-Rey, V El Khyari, S Rimet, O Bordas, B Guigal, N Braguer, D Seree, E Barra, Y Briand, C |
| description | We investigated the expression of c-
myc in HT29-D4, HBL100 and Caco-2 cells treated with microtubule stabilising (paclitaxel) or depolymerising agents (vinblastine, nocodazole). After induction by epidermal growth factor (EGF), c-
myc expression decreased in HT29-D4 cells treated with all the antimicrotubule agents. In HBL100 and Caco-2, when microtubules were stabilised with paclitaxel, c-
myc expression also decreased. In contrast, its expression increased after treatment with depolymerising agents. In both cell lines, we also observed that depolymerising agents alone induced c-
myc expression whilst paclitaxel had no effect. This mRNA induction was confirmed at the protein level. In HT29-D4, no variation of c-
myc expression was observed. Then, we showed that the increase of mRNA level was due to activation of gene transcription. These results indicate that modulation of c-
myc expression varied depending on the cell lines used and the type of antimicrotubule agents. This work provides a potential link between the microtubular network and c-
myc gene expression. |
| doi_str_mv | 10.1016/S0959-8049(00)00042-3 |
| format | Article |
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myc in HT29-D4, HBL100 and Caco-2 cells treated with microtubule stabilising (paclitaxel) or depolymerising agents (vinblastine, nocodazole). After induction by epidermal growth factor (EGF), c-
myc expression decreased in HT29-D4 cells treated with all the antimicrotubule agents. In HBL100 and Caco-2, when microtubules were stabilised with paclitaxel, c-
myc expression also decreased. In contrast, its expression increased after treatment with depolymerising agents. In both cell lines, we also observed that depolymerising agents alone induced c-
myc expression whilst paclitaxel had no effect. This mRNA induction was confirmed at the protein level. In HT29-D4, no variation of c-
myc expression was observed. Then, we showed that the increase of mRNA level was due to activation of gene transcription. These results indicate that modulation of c-
myc expression varied depending on the cell lines used and the type of antimicrotubule agents. This work provides a potential link between the microtubular network and c-
myc gene expression.</description><identifier>ISSN: 0959-8049</identifier><identifier>EISSN: 1879-0852</identifier><identifier>DOI: 10.1016/S0959-8049(00)00042-3</identifier><identifier>PMID: 10885610</identifier><language>eng</language><publisher>England: Elsevier Ltd</publisher><subject>Adenocarcinoma - drug therapy ; Antimicrotubule agents ; Blotting, Western ; c- myc ; c-myc gene ; Caco-2 Cells - metabolism ; Colonic Neoplasms - drug therapy ; Flow Cytometry ; Gene Expression Regulation, Neoplastic - drug effects ; Genes, myc - genetics ; HT29 Cells - metabolism ; Humans ; Microtubules - drug effects ; nocodazole ; Polymerase Chain Reaction - methods ; Proto-Oncogene Proteins c-myc - metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; RNA, Messenger - metabolism ; Transcription activation</subject><ispartof>European journal of cancer (1990), 2000-05, Vol.36 (8), p.1043-1049</ispartof><rights>2000 Elsevier Science Ltd</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c392t-6bdd3ab7fc6289d78fc379b02a483122638c2d206246e04fff008f4c3eda6cf13</citedby><cites>FETCH-LOGICAL-c392t-6bdd3ab7fc6289d78fc379b02a483122638c2d206246e04fff008f4c3eda6cf13</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0959804900000423$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10885610$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Bourgarel-Rey, V</creatorcontrib><creatorcontrib>El Khyari, S</creatorcontrib><creatorcontrib>Rimet, O</creatorcontrib><creatorcontrib>Bordas, B</creatorcontrib><creatorcontrib>Guigal, N</creatorcontrib><creatorcontrib>Braguer, D</creatorcontrib><creatorcontrib>Seree, E</creatorcontrib><creatorcontrib>Barra, Y</creatorcontrib><creatorcontrib>Briand, C</creatorcontrib><title>Opposite effects of antimicrotubule agents on c- myc oncogene expression depending on the cell lines used</title><title>European journal of cancer (1990)</title><addtitle>Eur J Cancer</addtitle><description>We investigated the expression of c-
myc in HT29-D4, HBL100 and Caco-2 cells treated with microtubule stabilising (paclitaxel) or depolymerising agents (vinblastine, nocodazole). After induction by epidermal growth factor (EGF), c-
myc expression decreased in HT29-D4 cells treated with all the antimicrotubule agents. In HBL100 and Caco-2, when microtubules were stabilised with paclitaxel, c-
myc expression also decreased. In contrast, its expression increased after treatment with depolymerising agents. In both cell lines, we also observed that depolymerising agents alone induced c-
myc expression whilst paclitaxel had no effect. This mRNA induction was confirmed at the protein level. In HT29-D4, no variation of c-
myc expression was observed. Then, we showed that the increase of mRNA level was due to activation of gene transcription. These results indicate that modulation of c-
myc expression varied depending on the cell lines used and the type of antimicrotubule agents. This work provides a potential link between the microtubular network and c-
myc gene expression.</description><subject>Adenocarcinoma - drug therapy</subject><subject>Antimicrotubule agents</subject><subject>Blotting, Western</subject><subject>c- myc</subject><subject>c-myc gene</subject><subject>Caco-2 Cells - metabolism</subject><subject>Colonic Neoplasms - drug therapy</subject><subject>Flow Cytometry</subject><subject>Gene Expression Regulation, Neoplastic - drug effects</subject><subject>Genes, myc - genetics</subject><subject>HT29 Cells - metabolism</subject><subject>Humans</subject><subject>Microtubules - drug effects</subject><subject>nocodazole</subject><subject>Polymerase Chain Reaction - methods</subject><subject>Proto-Oncogene Proteins c-myc - metabolism</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>RNA, Messenger - metabolism</subject><subject>Transcription activation</subject><issn>0959-8049</issn><issn>1879-0852</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2000</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkU1r3DAQhkVpaDab_oQGnUpzcDqSbFk6lRKaDwjsIc1Z2NIoVfFXLTt0_33k3SXkticNmuedGd6XkC8Mrhgw-f0RdKEzBbn-BnAJADnPxAeyYqrUGaiCfySrN-SUnMX4N0GlyuETOWWgVCEZrEjYDEMfw4QUvUc7Rdp7WnVTaIMd-2mu5wZp9Yzd0umozWi7tamyffpLov_DiDGG1HI4YOdC97xw0x-kFpuGNqHDSOeI7pyc-KqJ-PnwrsnTza_f13fZw-b2_vrnQ2aF5lMma-dEVZfeSq60K5W3otQ18CpXgnEuhbLccZA8lwi59x5A-dwKdJW0nok1-bqfO4z9vxnjZNoQl1uqDvs5mpJxIWTJj4KsLITWuUhgsQeTIzGO6M0whrYat4aBWcIwuzDM4rQBMLswzKK7OCyY6xbdO9Xe_QT82AOY_HgJOJpoA3YWXRhTFsb14ciKVyIbmk0</recordid><startdate>20000501</startdate><enddate>20000501</enddate><creator>Bourgarel-Rey, V</creator><creator>El Khyari, S</creator><creator>Rimet, O</creator><creator>Bordas, B</creator><creator>Guigal, N</creator><creator>Braguer, D</creator><creator>Seree, E</creator><creator>Barra, Y</creator><creator>Briand, C</creator><general>Elsevier Ltd</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>7TO</scope><scope>H94</scope><scope>7X8</scope></search><sort><creationdate>20000501</creationdate><title>Opposite effects of antimicrotubule agents on c- myc oncogene expression depending on the cell lines used</title><author>Bourgarel-Rey, V ; El Khyari, S ; Rimet, O ; Bordas, B ; Guigal, N ; Braguer, D ; Seree, E ; Barra, Y ; Briand, C</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c392t-6bdd3ab7fc6289d78fc379b02a483122638c2d206246e04fff008f4c3eda6cf13</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2000</creationdate><topic>Adenocarcinoma - drug therapy</topic><topic>Antimicrotubule agents</topic><topic>Blotting, Western</topic><topic>c- myc</topic><topic>c-myc gene</topic><topic>Caco-2 Cells - metabolism</topic><topic>Colonic Neoplasms - drug therapy</topic><topic>Flow Cytometry</topic><topic>Gene Expression Regulation, Neoplastic - drug effects</topic><topic>Genes, myc - genetics</topic><topic>HT29 Cells - metabolism</topic><topic>Humans</topic><topic>Microtubules - drug effects</topic><topic>nocodazole</topic><topic>Polymerase Chain Reaction - methods</topic><topic>Proto-Oncogene Proteins c-myc - metabolism</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>RNA, Messenger - metabolism</topic><topic>Transcription activation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Bourgarel-Rey, V</creatorcontrib><creatorcontrib>El Khyari, S</creatorcontrib><creatorcontrib>Rimet, O</creatorcontrib><creatorcontrib>Bordas, B</creatorcontrib><creatorcontrib>Guigal, N</creatorcontrib><creatorcontrib>Braguer, D</creatorcontrib><creatorcontrib>Seree, E</creatorcontrib><creatorcontrib>Barra, Y</creatorcontrib><creatorcontrib>Briand, C</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>European journal of cancer (1990)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Bourgarel-Rey, V</au><au>El Khyari, S</au><au>Rimet, O</au><au>Bordas, B</au><au>Guigal, N</au><au>Braguer, D</au><au>Seree, E</au><au>Barra, Y</au><au>Briand, C</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Opposite effects of antimicrotubule agents on c- myc oncogene expression depending on the cell lines used</atitle><jtitle>European journal of cancer (1990)</jtitle><addtitle>Eur J Cancer</addtitle><date>2000-05-01</date><risdate>2000</risdate><volume>36</volume><issue>8</issue><spage>1043</spage><epage>1049</epage><pages>1043-1049</pages><issn>0959-8049</issn><eissn>1879-0852</eissn><abstract>We investigated the expression of c-
myc in HT29-D4, HBL100 and Caco-2 cells treated with microtubule stabilising (paclitaxel) or depolymerising agents (vinblastine, nocodazole). After induction by epidermal growth factor (EGF), c-
myc expression decreased in HT29-D4 cells treated with all the antimicrotubule agents. In HBL100 and Caco-2, when microtubules were stabilised with paclitaxel, c-
myc expression also decreased. In contrast, its expression increased after treatment with depolymerising agents. In both cell lines, we also observed that depolymerising agents alone induced c-
myc expression whilst paclitaxel had no effect. This mRNA induction was confirmed at the protein level. In HT29-D4, no variation of c-
myc expression was observed. Then, we showed that the increase of mRNA level was due to activation of gene transcription. These results indicate that modulation of c-
myc expression varied depending on the cell lines used and the type of antimicrotubule agents. This work provides a potential link between the microtubular network and c-
myc gene expression.</abstract><cop>England</cop><pub>Elsevier Ltd</pub><pmid>10885610</pmid><doi>10.1016/S0959-8049(00)00042-3</doi><tpages>7</tpages></addata></record> |
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| identifier | ISSN: 0959-8049 |
| ispartof | European journal of cancer (1990), 2000-05, Vol.36 (8), p.1043-1049 |
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| source | MEDLINE; Elsevier ScienceDirect Journals |
| subjects | Adenocarcinoma - drug therapy Antimicrotubule agents Blotting, Western c- myc c-myc gene Caco-2 Cells - metabolism Colonic Neoplasms - drug therapy Flow Cytometry Gene Expression Regulation, Neoplastic - drug effects Genes, myc - genetics HT29 Cells - metabolism Humans Microtubules - drug effects nocodazole Polymerase Chain Reaction - methods Proto-Oncogene Proteins c-myc - metabolism Reverse Transcriptase Polymerase Chain Reaction RNA, Messenger - metabolism Transcription activation |
| title | Opposite effects of antimicrotubule agents on c- myc oncogene expression depending on the cell lines used |
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