Oncogenic ras alters sensitivity of mouse colonocytes to butyrate and fatty acid mediated growth arrest and apoptosis
Docosahexaenoic acid (DHA) and butyrate favorably modulate colonocyte proliferation and apoptosis. In order to elucidate how oncogenic Ras modulates responses to these chemopreventive nutrients, we incubated isogenic non-transformed and Ras malignant transformed mouse colon cells with butyrate and D...
Gespeichert in:
| Veröffentlicht in: | Cancer letters 2002-12, Vol.186 (1), p.29-35 |
|---|---|
| Hauptverfasser: | , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 35 |
|---|---|
| container_issue | 1 |
| container_start_page | 29 |
| container_title | Cancer letters |
| container_volume | 186 |
| creator | Turner, Nancy D Zhang, Jianhu Davidson, Laurie A Lupton, Joanne R Chapkin, Robert S |
| description | Docosahexaenoic acid (DHA) and butyrate favorably modulate colonocyte proliferation and apoptosis. In order to elucidate how oncogenic Ras modulates responses to these chemopreventive nutrients, we incubated isogenic non-transformed and Ras malignant transformed mouse colon cells with butyrate and DHA or linoleic acid (LA). Combining DHA with 1
mM butyrate decreased proliferation relative to LA or no PUFA treatment in both cell lines. At a higher butyrate dose (5
mM), caspase 3 activity was elevated to a greater extent in Ras transformed cells. Only non-transformed cells were sensitive to the apoptogenic effects of DHA, indicating that Ras transformation alters sensitivity to dietary chemopreventive agents. |
| doi_str_mv | 10.1016/S0304-3835(02)00325-7 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_72016652</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>S0304383502003257</els_id><sourcerecordid>3241471321</sourcerecordid><originalsourceid>FETCH-LOGICAL-c450t-da0515827b60bd07bde6e85b7194214bb5d62a28fe921548fc70a226c9fdea813</originalsourceid><addsrcrecordid>eNqF0d9rFDEQB_AgFnut_glKQCz6sHWS3WyyTyLFH4VCH6rPIZvM1pS95EyylfvvTe8OC770KRA-M8zMl5DXDM4ZsP7jDbTQNa1qxXvgHwBaLhr5jKyYkryRg4LnZPWPHJOTnO8AQHRSvCDHjDPVguQrslwHG28xeEuTydTMBVOmGUP2xd_7sqVxouu4ZKQ2zjFEuy2YaYl0XMo2mYLUBEcnUyo11ju6Rufrt6O3Kf4pv6hJCXPZKbOJmxKzzy_J0WTmjK8O7yn5-fXLj4vvzdX1t8uLz1eN7QSUxhkQTCguxx5GB3J02KMSo2RDx1k3jsL13HA14cCZ6NRkJRjOeztMDo1i7Sk52_fdpPh7qWPotc8W59kErDtpyespe8GfhEwJELxTFb79D97FJYW6hGaVtD2vN69K7JVNMeeEk94kvzZpqxnoh_j0Lj79kI0GrnfxaVnr3hy6L2O942PVIa8K3h2AydbMUzLB-vzoum7ggxiq-7R3WK977zHpbD0GW7NJaIt20T8xyl8u37ed</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1505362304</pqid></control><display><type>article</type><title>Oncogenic ras alters sensitivity of mouse colonocytes to butyrate and fatty acid mediated growth arrest and apoptosis</title><source>MEDLINE</source><source>ScienceDirect Journals (5 years ago - present)</source><creator>Turner, Nancy D ; Zhang, Jianhu ; Davidson, Laurie A ; Lupton, Joanne R ; Chapkin, Robert S</creator><creatorcontrib>Turner, Nancy D ; Zhang, Jianhu ; Davidson, Laurie A ; Lupton, Joanne R ; Chapkin, Robert S</creatorcontrib><description>Docosahexaenoic acid (DHA) and butyrate favorably modulate colonocyte proliferation and apoptosis. In order to elucidate how oncogenic Ras modulates responses to these chemopreventive nutrients, we incubated isogenic non-transformed and Ras malignant transformed mouse colon cells with butyrate and DHA or linoleic acid (LA). Combining DHA with 1
mM butyrate decreased proliferation relative to LA or no PUFA treatment in both cell lines. At a higher butyrate dose (5
mM), caspase 3 activity was elevated to a greater extent in Ras transformed cells. Only non-transformed cells were sensitive to the apoptogenic effects of DHA, indicating that Ras transformation alters sensitivity to dietary chemopreventive agents.</description><identifier>ISSN: 0304-3835</identifier><identifier>EISSN: 1872-7980</identifier><identifier>DOI: 10.1016/S0304-3835(02)00325-7</identifier><identifier>PMID: 12183072</identifier><identifier>CODEN: CALEDQ</identifier><language>eng</language><publisher>Shannon: Elsevier Ireland Ltd</publisher><subject>Animals ; Antineoplastic agents ; Apoptosis ; Apoptosis - drug effects ; Biological and medical sciences ; Butyrate ; Butyrates - pharmacology ; Cell culture ; Cell Division - drug effects ; Cell growth ; Chemotherapy ; Colon - cytology ; Colon - drug effects ; Colon cancer ; Colorectal cancer ; Deoxyribonucleic acid ; Dietary fiber ; Dissemination ; DNA ; DNA Adducts - metabolism ; Docosahexaenoic acid ; Docosahexaenoic Acids - pharmacology ; Dose-Response Relationship, Drug ; Experiments ; Fatty acids ; Fatty Acids, Omega-3 ; Fatty Acids, Unsaturated - pharmacology ; Fish oils ; Genes, ras - physiology ; Linoleic acid ; Linoleic Acid - pharmacology ; Medical sciences ; Mice ; Pharmacology. Drug treatments ; Proliferation ; Ras ; Space life sciences ; Triglycerides - pharmacology ; Tumor cell ; Tumors</subject><ispartof>Cancer letters, 2002-12, Vol.186 (1), p.29-35</ispartof><rights>2002 Elsevier Science Ireland Ltd</rights><rights>2003 INIST-CNRS</rights><rights>Copyright Elsevier Limited Dec 1, 2002</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c450t-da0515827b60bd07bde6e85b7194214bb5d62a28fe921548fc70a226c9fdea813</citedby><cites>FETCH-LOGICAL-c450t-da0515827b60bd07bde6e85b7194214bb5d62a28fe921548fc70a226c9fdea813</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/S0304-3835(02)00325-7$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=14492959$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12183072$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Turner, Nancy D</creatorcontrib><creatorcontrib>Zhang, Jianhu</creatorcontrib><creatorcontrib>Davidson, Laurie A</creatorcontrib><creatorcontrib>Lupton, Joanne R</creatorcontrib><creatorcontrib>Chapkin, Robert S</creatorcontrib><title>Oncogenic ras alters sensitivity of mouse colonocytes to butyrate and fatty acid mediated growth arrest and apoptosis</title><title>Cancer letters</title><addtitle>Cancer Lett</addtitle><description>Docosahexaenoic acid (DHA) and butyrate favorably modulate colonocyte proliferation and apoptosis. In order to elucidate how oncogenic Ras modulates responses to these chemopreventive nutrients, we incubated isogenic non-transformed and Ras malignant transformed mouse colon cells with butyrate and DHA or linoleic acid (LA). Combining DHA with 1
mM butyrate decreased proliferation relative to LA or no PUFA treatment in both cell lines. At a higher butyrate dose (5
mM), caspase 3 activity was elevated to a greater extent in Ras transformed cells. Only non-transformed cells were sensitive to the apoptogenic effects of DHA, indicating that Ras transformation alters sensitivity to dietary chemopreventive agents.</description><subject>Animals</subject><subject>Antineoplastic agents</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Biological and medical sciences</subject><subject>Butyrate</subject><subject>Butyrates - pharmacology</subject><subject>Cell culture</subject><subject>Cell Division - drug effects</subject><subject>Cell growth</subject><subject>Chemotherapy</subject><subject>Colon - cytology</subject><subject>Colon - drug effects</subject><subject>Colon cancer</subject><subject>Colorectal cancer</subject><subject>Deoxyribonucleic acid</subject><subject>Dietary fiber</subject><subject>Dissemination</subject><subject>DNA</subject><subject>DNA Adducts - metabolism</subject><subject>Docosahexaenoic acid</subject><subject>Docosahexaenoic Acids - pharmacology</subject><subject>Dose-Response Relationship, Drug</subject><subject>Experiments</subject><subject>Fatty acids</subject><subject>Fatty Acids, Omega-3</subject><subject>Fatty Acids, Unsaturated - pharmacology</subject><subject>Fish oils</subject><subject>Genes, ras - physiology</subject><subject>Linoleic acid</subject><subject>Linoleic Acid - pharmacology</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Pharmacology. Drug treatments</subject><subject>Proliferation</subject><subject>Ras</subject><subject>Space life sciences</subject><subject>Triglycerides - pharmacology</subject><subject>Tumor cell</subject><subject>Tumors</subject><issn>0304-3835</issn><issn>1872-7980</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqF0d9rFDEQB_AgFnut_glKQCz6sHWS3WyyTyLFH4VCH6rPIZvM1pS95EyylfvvTe8OC770KRA-M8zMl5DXDM4ZsP7jDbTQNa1qxXvgHwBaLhr5jKyYkryRg4LnZPWPHJOTnO8AQHRSvCDHjDPVguQrslwHG28xeEuTydTMBVOmGUP2xd_7sqVxouu4ZKQ2zjFEuy2YaYl0XMo2mYLUBEcnUyo11ju6Rufrt6O3Kf4pv6hJCXPZKbOJmxKzzy_J0WTmjK8O7yn5-fXLj4vvzdX1t8uLz1eN7QSUxhkQTCguxx5GB3J02KMSo2RDx1k3jsL13HA14cCZ6NRkJRjOeztMDo1i7Sk52_fdpPh7qWPotc8W59kErDtpyespe8GfhEwJELxTFb79D97FJYW6hGaVtD2vN69K7JVNMeeEk94kvzZpqxnoh_j0Lj79kI0GrnfxaVnr3hy6L2O942PVIa8K3h2AydbMUzLB-vzoum7ggxiq-7R3WK977zHpbD0GW7NJaIt20T8xyl8u37ed</recordid><startdate>20021201</startdate><enddate>20021201</enddate><creator>Turner, Nancy D</creator><creator>Zhang, Jianhu</creator><creator>Davidson, Laurie A</creator><creator>Lupton, Joanne R</creator><creator>Chapkin, Robert S</creator><general>Elsevier Ireland Ltd</general><general>Elsevier</general><general>Elsevier Limited</general><scope>IQODW</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>7TO</scope><scope>7U9</scope><scope>H94</scope><scope>K9.</scope><scope>NAPCQ</scope><scope>7X8</scope></search><sort><creationdate>20021201</creationdate><title>Oncogenic ras alters sensitivity of mouse colonocytes to butyrate and fatty acid mediated growth arrest and apoptosis</title><author>Turner, Nancy D ; Zhang, Jianhu ; Davidson, Laurie A ; Lupton, Joanne R ; Chapkin, Robert S</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c450t-da0515827b60bd07bde6e85b7194214bb5d62a28fe921548fc70a226c9fdea813</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Animals</topic><topic>Antineoplastic agents</topic><topic>Apoptosis</topic><topic>Apoptosis - drug effects</topic><topic>Biological and medical sciences</topic><topic>Butyrate</topic><topic>Butyrates - pharmacology</topic><topic>Cell culture</topic><topic>Cell Division - drug effects</topic><topic>Cell growth</topic><topic>Chemotherapy</topic><topic>Colon - cytology</topic><topic>Colon - drug effects</topic><topic>Colon cancer</topic><topic>Colorectal cancer</topic><topic>Deoxyribonucleic acid</topic><topic>Dietary fiber</topic><topic>Dissemination</topic><topic>DNA</topic><topic>DNA Adducts - metabolism</topic><topic>Docosahexaenoic acid</topic><topic>Docosahexaenoic Acids - pharmacology</topic><topic>Dose-Response Relationship, Drug</topic><topic>Experiments</topic><topic>Fatty acids</topic><topic>Fatty Acids, Omega-3</topic><topic>Fatty Acids, Unsaturated - pharmacology</topic><topic>Fish oils</topic><topic>Genes, ras - physiology</topic><topic>Linoleic acid</topic><topic>Linoleic Acid - pharmacology</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Pharmacology. Drug treatments</topic><topic>Proliferation</topic><topic>Ras</topic><topic>Space life sciences</topic><topic>Triglycerides - pharmacology</topic><topic>Tumor cell</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Turner, Nancy D</creatorcontrib><creatorcontrib>Zhang, Jianhu</creatorcontrib><creatorcontrib>Davidson, Laurie A</creatorcontrib><creatorcontrib>Lupton, Joanne R</creatorcontrib><creatorcontrib>Chapkin, Robert S</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>CrossRef</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>MEDLINE - Academic</collection><jtitle>Cancer letters</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Turner, Nancy D</au><au>Zhang, Jianhu</au><au>Davidson, Laurie A</au><au>Lupton, Joanne R</au><au>Chapkin, Robert S</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Oncogenic ras alters sensitivity of mouse colonocytes to butyrate and fatty acid mediated growth arrest and apoptosis</atitle><jtitle>Cancer letters</jtitle><addtitle>Cancer Lett</addtitle><date>2002-12-01</date><risdate>2002</risdate><volume>186</volume><issue>1</issue><spage>29</spage><epage>35</epage><pages>29-35</pages><issn>0304-3835</issn><eissn>1872-7980</eissn><coden>CALEDQ</coden><abstract>Docosahexaenoic acid (DHA) and butyrate favorably modulate colonocyte proliferation and apoptosis. In order to elucidate how oncogenic Ras modulates responses to these chemopreventive nutrients, we incubated isogenic non-transformed and Ras malignant transformed mouse colon cells with butyrate and DHA or linoleic acid (LA). Combining DHA with 1
mM butyrate decreased proliferation relative to LA or no PUFA treatment in both cell lines. At a higher butyrate dose (5
mM), caspase 3 activity was elevated to a greater extent in Ras transformed cells. Only non-transformed cells were sensitive to the apoptogenic effects of DHA, indicating that Ras transformation alters sensitivity to dietary chemopreventive agents.</abstract><cop>Shannon</cop><pub>Elsevier Ireland Ltd</pub><pmid>12183072</pmid><doi>10.1016/S0304-3835(02)00325-7</doi><tpages>7</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0304-3835 |
| ispartof | Cancer letters, 2002-12, Vol.186 (1), p.29-35 |
| issn | 0304-3835 1872-7980 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_72016652 |
| source | MEDLINE; ScienceDirect Journals (5 years ago - present) |
| subjects | Animals Antineoplastic agents Apoptosis Apoptosis - drug effects Biological and medical sciences Butyrate Butyrates - pharmacology Cell culture Cell Division - drug effects Cell growth Chemotherapy Colon - cytology Colon - drug effects Colon cancer Colorectal cancer Deoxyribonucleic acid Dietary fiber Dissemination DNA DNA Adducts - metabolism Docosahexaenoic acid Docosahexaenoic Acids - pharmacology Dose-Response Relationship, Drug Experiments Fatty acids Fatty Acids, Omega-3 Fatty Acids, Unsaturated - pharmacology Fish oils Genes, ras - physiology Linoleic acid Linoleic Acid - pharmacology Medical sciences Mice Pharmacology. Drug treatments Proliferation Ras Space life sciences Triglycerides - pharmacology Tumor cell Tumors |
| title | Oncogenic ras alters sensitivity of mouse colonocytes to butyrate and fatty acid mediated growth arrest and apoptosis |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-07T23%3A15%3A26IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Oncogenic%20ras%20alters%20sensitivity%20of%20mouse%20colonocytes%20to%20butyrate%20and%20fatty%20acid%20mediated%20growth%20arrest%20and%20apoptosis&rft.jtitle=Cancer%20letters&rft.au=Turner,%20Nancy%20D&rft.date=2002-12-01&rft.volume=186&rft.issue=1&rft.spage=29&rft.epage=35&rft.pages=29-35&rft.issn=0304-3835&rft.eissn=1872-7980&rft.coden=CALEDQ&rft_id=info:doi/10.1016/S0304-3835(02)00325-7&rft_dat=%3Cproquest_cross%3E3241471321%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1505362304&rft_id=info:pmid/12183072&rft_els_id=S0304383502003257&rfr_iscdi=true |