A Prenylation Inhibitor (Sodium Phenylacetate) Differently Affects MCF-7 Cell Death when ras is Overexpressed, Partly Involving P42/44, JNK and P38 Kinase Activations
Background: Sodium phenylacetate (NaPa) inhibits breast cancer cell proliferation decreasing prenylation of small G proteins including Ras. Materials and Methods: Aponecrosis induced by NaPa in MCF-7 and MCF-7ras breast cancer cells was evaluated by measuring Annexin V/PI labelling by flow cytometry...
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| Veröffentlicht in: | Anticancer research 2008-03, Vol.28 (2A), p.1029-1037 |
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| creator | DI BENEDETTO, Mélanie CREPIN, Michel KRAEMER, Michel OUDAR, Olivier |
| description | Background: Sodium phenylacetate (NaPa) inhibits breast cancer cell proliferation decreasing prenylation of small G proteins
including Ras. Materials and Methods: Aponecrosis induced by NaPa in MCF-7 and MCF-7ras breast cancer cells was evaluated
by measuring Annexin V/PI labelling by flow cytometry. Specific inhibitors of p42/44 (PD 98059), p38 (SB 600125) and JNK (SP
202190) in association with NaPa were also tested. Mitogen-activated kinase (MAPK) activation was measured by immunoprecipitation.
Results: NaPa induced cell death more efficiently (80%) in the MCF-7ras cells compared to the MCF-7 cells (60%). NaPa activated
ERK 1/2 and its combination with PD 98059 decreased cell death in the MCF-7ras cells in contrast to the MCF-7 cells. Combination
of NaPa with specific inhibitors of both JNK and p38 kinases also partly decreased MCF-7ras cell death. Conclusion: NaPa induced
cell death differently when ras was overexpressed in breast cancer cells, partly involving p42/44, JNK and p38 pathways. |
| format | Article |
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including Ras. Materials and Methods: Aponecrosis induced by NaPa in MCF-7 and MCF-7ras breast cancer cells was evaluated
by measuring Annexin V/PI labelling by flow cytometry. Specific inhibitors of p42/44 (PD 98059), p38 (SB 600125) and JNK (SP
202190) in association with NaPa were also tested. Mitogen-activated kinase (MAPK) activation was measured by immunoprecipitation.
Results: NaPa induced cell death more efficiently (80%) in the MCF-7ras cells compared to the MCF-7 cells (60%). NaPa activated
ERK 1/2 and its combination with PD 98059 decreased cell death in the MCF-7ras cells in contrast to the MCF-7 cells. Combination
of NaPa with specific inhibitors of both JNK and p38 kinases also partly decreased MCF-7ras cell death. Conclusion: NaPa induced
cell death differently when ras was overexpressed in breast cancer cells, partly involving p42/44, JNK and p38 pathways.</description><identifier>ISSN: 0250-7005</identifier><identifier>EISSN: 1791-7530</identifier><identifier>PMID: 18507051</identifier><language>eng</language><publisher>Attiki: International Institute of Anticancer Research</publisher><subject>Animals ; Apoptosis - drug effects ; Biological and medical sciences ; Cell Line, Tumor ; Flavonoids - pharmacology ; Genes, ras ; JNK Mitogen-Activated Protein Kinases - metabolism ; Medical sciences ; Mice ; Mitogen-Activated Protein Kinase 1 - metabolism ; Mitogen-Activated Protein Kinase 3 - metabolism ; p38 Mitogen-Activated Protein Kinases - metabolism ; Phenylacetates - pharmacology ; Proto-Oncogene Proteins p21(ras) - metabolism ; Tumors</subject><ispartof>Anticancer research, 2008-03, Vol.28 (2A), p.1029-1037</ispartof><rights>2008 INIST-CNRS</rights><rights>Distributed under a Creative Commons Attribution 4.0 International License</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,776,780,881</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=20290487$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18507051$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://hal.science/hal-00416613$$DView record in HAL$$Hfree_for_read</backlink></links><search><creatorcontrib>DI BENEDETTO, Mélanie</creatorcontrib><creatorcontrib>CREPIN, Michel</creatorcontrib><creatorcontrib>KRAEMER, Michel</creatorcontrib><creatorcontrib>OUDAR, Olivier</creatorcontrib><title>A Prenylation Inhibitor (Sodium Phenylacetate) Differently Affects MCF-7 Cell Death when ras is Overexpressed, Partly Involving P42/44, JNK and P38 Kinase Activations</title><title>Anticancer research</title><addtitle>Anticancer Res</addtitle><description>Background: Sodium phenylacetate (NaPa) inhibits breast cancer cell proliferation decreasing prenylation of small G proteins
including Ras. Materials and Methods: Aponecrosis induced by NaPa in MCF-7 and MCF-7ras breast cancer cells was evaluated
by measuring Annexin V/PI labelling by flow cytometry. Specific inhibitors of p42/44 (PD 98059), p38 (SB 600125) and JNK (SP
202190) in association with NaPa were also tested. Mitogen-activated kinase (MAPK) activation was measured by immunoprecipitation.
Results: NaPa induced cell death more efficiently (80%) in the MCF-7ras cells compared to the MCF-7 cells (60%). NaPa activated
ERK 1/2 and its combination with PD 98059 decreased cell death in the MCF-7ras cells in contrast to the MCF-7 cells. Combination
of NaPa with specific inhibitors of both JNK and p38 kinases also partly decreased MCF-7ras cell death. Conclusion: NaPa induced
cell death differently when ras was overexpressed in breast cancer cells, partly involving p42/44, JNK and p38 pathways.</description><subject>Animals</subject><subject>Apoptosis - drug effects</subject><subject>Biological and medical sciences</subject><subject>Cell Line, Tumor</subject><subject>Flavonoids - pharmacology</subject><subject>Genes, ras</subject><subject>JNK Mitogen-Activated Protein Kinases - metabolism</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mitogen-Activated Protein Kinase 1 - metabolism</subject><subject>Mitogen-Activated Protein Kinase 3 - metabolism</subject><subject>p38 Mitogen-Activated Protein Kinases - metabolism</subject><subject>Phenylacetates - pharmacology</subject><subject>Proto-Oncogene Proteins p21(ras) - metabolism</subject><subject>Tumors</subject><issn>0250-7005</issn><issn>1791-7530</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkdtu1DAQhiMEokvhFdDcgKjUCDu2c7iMtrRdutBI5d4aJ05j5CRb27tlX6jPidsu5cojz_f_c3qVLGhR0bQQjLxOFiQTJC0IEUfJO-9_E5LnVcneJke0FKQggi6Shxoap6e9xWDmCVbTYJQJs4MvN3NntiM0w1O21QGDPoEz0_c6CoLdQx3DNnj4sTxPC1hqa-FMYxjgPmrAoQfj4XoX8T8bp73X3Sk06B6lq2k3252ZbqHh2VfOT-H7zyvAqYOGlXBlJvQa6jaY3VNf_n3ypkfr9YfDe5zcnH_7tbxM19cXq2W9TgdGeEh7kVNBKRMCteYZJwK5VoSgVm2HQmdcqbLIVUY7RlXVsaoURalaReMkLTtOTp5dB7Ry48yIbi9nNPKyXsvHP0I4zXPKdjSyn5_ZjZvvttoHORrfxh3gpOetlwUp4uZZGcGPB3CrRt29-P67QQQ-HQD0Ldre4dQa_8JlJKsIL4v_FQdzO9wbp6Uf0dpoyyS6rJRZLWmE2V9OVZye</recordid><startdate>20080301</startdate><enddate>20080301</enddate><creator>DI BENEDETTO, Mélanie</creator><creator>CREPIN, Michel</creator><creator>KRAEMER, Michel</creator><creator>OUDAR, Olivier</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><scope>7X8</scope><scope>1XC</scope></search><sort><creationdate>20080301</creationdate><title>A Prenylation Inhibitor (Sodium Phenylacetate) Differently Affects MCF-7 Cell Death when ras is Overexpressed, Partly Involving P42/44, JNK and P38 Kinase Activations</title><author>DI BENEDETTO, Mélanie ; CREPIN, Michel ; KRAEMER, Michel ; OUDAR, Olivier</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-h304t-f561511355aee42405a4eb00aebcda5e24bb876b21d31b9d398578bcb1fecc3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Animals</topic><topic>Apoptosis - drug effects</topic><topic>Biological and medical sciences</topic><topic>Cell Line, Tumor</topic><topic>Flavonoids - pharmacology</topic><topic>Genes, ras</topic><topic>JNK Mitogen-Activated Protein Kinases - metabolism</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mitogen-Activated Protein Kinase 1 - metabolism</topic><topic>Mitogen-Activated Protein Kinase 3 - metabolism</topic><topic>p38 Mitogen-Activated Protein Kinases - metabolism</topic><topic>Phenylacetates - pharmacology</topic><topic>Proto-Oncogene Proteins p21(ras) - metabolism</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>DI BENEDETTO, Mélanie</creatorcontrib><creatorcontrib>CREPIN, Michel</creatorcontrib><creatorcontrib>KRAEMER, Michel</creatorcontrib><creatorcontrib>OUDAR, Olivier</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><collection>Hyper Article en Ligne (HAL)</collection><jtitle>Anticancer research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>DI BENEDETTO, Mélanie</au><au>CREPIN, Michel</au><au>KRAEMER, Michel</au><au>OUDAR, Olivier</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>A Prenylation Inhibitor (Sodium Phenylacetate) Differently Affects MCF-7 Cell Death when ras is Overexpressed, Partly Involving P42/44, JNK and P38 Kinase Activations</atitle><jtitle>Anticancer research</jtitle><addtitle>Anticancer Res</addtitle><date>2008-03-01</date><risdate>2008</risdate><volume>28</volume><issue>2A</issue><spage>1029</spage><epage>1037</epage><pages>1029-1037</pages><issn>0250-7005</issn><eissn>1791-7530</eissn><abstract>Background: Sodium phenylacetate (NaPa) inhibits breast cancer cell proliferation decreasing prenylation of small G proteins
including Ras. Materials and Methods: Aponecrosis induced by NaPa in MCF-7 and MCF-7ras breast cancer cells was evaluated
by measuring Annexin V/PI labelling by flow cytometry. Specific inhibitors of p42/44 (PD 98059), p38 (SB 600125) and JNK (SP
202190) in association with NaPa were also tested. Mitogen-activated kinase (MAPK) activation was measured by immunoprecipitation.
Results: NaPa induced cell death more efficiently (80%) in the MCF-7ras cells compared to the MCF-7 cells (60%). NaPa activated
ERK 1/2 and its combination with PD 98059 decreased cell death in the MCF-7ras cells in contrast to the MCF-7 cells. Combination
of NaPa with specific inhibitors of both JNK and p38 kinases also partly decreased MCF-7ras cell death. Conclusion: NaPa induced
cell death differently when ras was overexpressed in breast cancer cells, partly involving p42/44, JNK and p38 pathways.</abstract><cop>Attiki</cop><pub>International Institute of Anticancer Research</pub><pmid>18507051</pmid><tpages>9</tpages></addata></record> |
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| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals |
| subjects | Animals Apoptosis - drug effects Biological and medical sciences Cell Line, Tumor Flavonoids - pharmacology Genes, ras JNK Mitogen-Activated Protein Kinases - metabolism Medical sciences Mice Mitogen-Activated Protein Kinase 1 - metabolism Mitogen-Activated Protein Kinase 3 - metabolism p38 Mitogen-Activated Protein Kinases - metabolism Phenylacetates - pharmacology Proto-Oncogene Proteins p21(ras) - metabolism Tumors |
| title | A Prenylation Inhibitor (Sodium Phenylacetate) Differently Affects MCF-7 Cell Death when ras is Overexpressed, Partly Involving P42/44, JNK and P38 Kinase Activations |
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