9-Hydroxystearic acid interferes with EGF signalling in a human colon adenocarcinoma
The epidermal growth factor has long been known to be strictly correlated with the highly proliferating activities of cancer cells and primary tumors. Moreover, in the nucleus, the epidermal growth factor/epidermal growth factor receptor complex (EGF/EGFR) functions as a transcriptional regulator th...
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Veröffentlicht in: | Biochemical and biophysical research communications 2006-04, Vol.342 (2), p.585-588 |
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creator | Calonghi, Natalia Pagnotta, Eleonora Parolin, Carola Tognoli, Cristina Boga, Carla Masotti, Lanfranco |
description | The epidermal growth factor has long been known to be strictly correlated with the highly proliferating activities of cancer cells and primary tumors. Moreover, in the nucleus, the epidermal growth factor/epidermal growth factor receptor complex (EGF/EGFR) functions as a transcriptional regulator that activates the
cyclin D1 gene. 9-hydroxystearic acid (9-HSA) induces cell proliferation arrest and differentiation in HT29 colon cancer cells by inhibiting histone deacetylase 1 (HDAC1). 9-HSA-treated HT29, when stimulated with EGF, are not responsive and surprisingly undergo a further arrest. In order to understand the mechanisms of this effect, we analyzed the degree of internalization of the EGF/EGFR complex and its interactions with HDAC1. It appears that HDAC1, as modified by 9-HSA, is unable to associate with cyclin D1, interfering with the cell proliferation program, and sequesters the EGF/EGFR complex interrupting the transduction of the mitogenic signal. |
doi_str_mv | 10.1016/j.bbrc.2006.02.008 |
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cyclin D1 gene. 9-hydroxystearic acid (9-HSA) induces cell proliferation arrest and differentiation in HT29 colon cancer cells by inhibiting histone deacetylase 1 (HDAC1). 9-HSA-treated HT29, when stimulated with EGF, are not responsive and surprisingly undergo a further arrest. In order to understand the mechanisms of this effect, we analyzed the degree of internalization of the EGF/EGFR complex and its interactions with HDAC1. It appears that HDAC1, as modified by 9-HSA, is unable to associate with cyclin D1, interfering with the cell proliferation program, and sequesters the EGF/EGFR complex interrupting the transduction of the mitogenic signal.</description><identifier>ISSN: 0006-291X</identifier><identifier>EISSN: 1090-2104</identifier><identifier>DOI: 10.1016/j.bbrc.2006.02.008</identifier><identifier>PMID: 16487928</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>60 APPLIED LIFE SCIENCES ; 9-HSA ; Adenocarcinoma - metabolism ; Adenocarcinoma - pathology ; ALBUMINS ; BLOOD SERUM ; CARCINOMAS ; CELL NUCLEI ; CELL PROLIFERATION ; Cell Proliferation - drug effects ; Colon cancer cell ; Colonic Neoplasms - metabolism ; Colonic Neoplasms - pathology ; Cyclin D1 ; Cyclin D1 - antagonists & inhibitors ; Cyclin D1 - biosynthesis ; Cyclin D1 - genetics ; EGFR ; Epidermal Growth Factor - antagonists & inhibitors ; Epidermal Growth Factor - pharmacology ; Epidermal Growth Factor - physiology ; Fluorescent Antibody Technique ; GENES ; GROWTH FACTORS ; HDAC1 ; Histone Deacetylase 1 ; Histone Deacetylases - metabolism ; HT29 Cells ; Humans ; LARGE INTESTINE ; Receptor, Epidermal Growth Factor - metabolism ; RECEPTORS ; Signal Transduction - drug effects ; Stearic Acids - pharmacology</subject><ispartof>Biochemical and biophysical research communications, 2006-04, Vol.342 (2), p.585-588</ispartof><rights>2006 Elsevier Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c382t-5fce67a57191e7e96f0551945045cdb1eb664d6b4fd6a2a7137cf4a1c8ddb5783</citedby><cites>FETCH-LOGICAL-c382t-5fce67a57191e7e96f0551945045cdb1eb664d6b4fd6a2a7137cf4a1c8ddb5783</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.bbrc.2006.02.008$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>230,314,780,784,885,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16487928$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://www.osti.gov/biblio/20798882$$D View this record in Osti.gov$$Hfree_for_read</backlink></links><search><creatorcontrib>Calonghi, Natalia</creatorcontrib><creatorcontrib>Pagnotta, Eleonora</creatorcontrib><creatorcontrib>Parolin, Carola</creatorcontrib><creatorcontrib>Tognoli, Cristina</creatorcontrib><creatorcontrib>Boga, Carla</creatorcontrib><creatorcontrib>Masotti, Lanfranco</creatorcontrib><title>9-Hydroxystearic acid interferes with EGF signalling in a human colon adenocarcinoma</title><title>Biochemical and biophysical research communications</title><addtitle>Biochem Biophys Res Commun</addtitle><description>The epidermal growth factor has long been known to be strictly correlated with the highly proliferating activities of cancer cells and primary tumors. Moreover, in the nucleus, the epidermal growth factor/epidermal growth factor receptor complex (EGF/EGFR) functions as a transcriptional regulator that activates the
cyclin D1 gene. 9-hydroxystearic acid (9-HSA) induces cell proliferation arrest and differentiation in HT29 colon cancer cells by inhibiting histone deacetylase 1 (HDAC1). 9-HSA-treated HT29, when stimulated with EGF, are not responsive and surprisingly undergo a further arrest. In order to understand the mechanisms of this effect, we analyzed the degree of internalization of the EGF/EGFR complex and its interactions with HDAC1. It appears that HDAC1, as modified by 9-HSA, is unable to associate with cyclin D1, interfering with the cell proliferation program, and sequesters the EGF/EGFR complex interrupting the transduction of the mitogenic signal.</description><subject>60 APPLIED LIFE SCIENCES</subject><subject>9-HSA</subject><subject>Adenocarcinoma - metabolism</subject><subject>Adenocarcinoma - pathology</subject><subject>ALBUMINS</subject><subject>BLOOD SERUM</subject><subject>CARCINOMAS</subject><subject>CELL NUCLEI</subject><subject>CELL PROLIFERATION</subject><subject>Cell Proliferation - drug effects</subject><subject>Colon cancer cell</subject><subject>Colonic Neoplasms - metabolism</subject><subject>Colonic Neoplasms - pathology</subject><subject>Cyclin D1</subject><subject>Cyclin D1 - antagonists & inhibitors</subject><subject>Cyclin D1 - biosynthesis</subject><subject>Cyclin D1 - genetics</subject><subject>EGFR</subject><subject>Epidermal Growth Factor - antagonists & inhibitors</subject><subject>Epidermal Growth Factor - pharmacology</subject><subject>Epidermal Growth Factor - physiology</subject><subject>Fluorescent Antibody Technique</subject><subject>GENES</subject><subject>GROWTH FACTORS</subject><subject>HDAC1</subject><subject>Histone Deacetylase 1</subject><subject>Histone Deacetylases - metabolism</subject><subject>HT29 Cells</subject><subject>Humans</subject><subject>LARGE INTESTINE</subject><subject>Receptor, Epidermal Growth Factor - metabolism</subject><subject>RECEPTORS</subject><subject>Signal Transduction - drug effects</subject><subject>Stearic Acids - pharmacology</subject><issn>0006-291X</issn><issn>1090-2104</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kE2LFDEQhoMo7rj6BzxIg-Ct2yTT-QIvsuyHsOBlBW8hXaneydCdrEnP6vx708yAN09FUc_7UjyEvGe0Y5TJz_tuGDJ0nFLZUd5Rql-QDaOGtpzR_iXZ0HppuWE_L8ibUvaUMtZL85pcMNlrZbjekAfT3h19Tn-OZUGXAzQOgm9CXDCPmLE0v8Oya65vb5oSHqObphAf67lxze4wu9hAmlLdPMYELkOIaXZvyavRTQXfnecl-XFz_XB1195_v_129fW-ha3mSytGQKmcUMwwVGjkSIVgphe0F-AHhoOUvZdDP3rpuFNsq2DsHQPt_SCU3l6Sj6feVJZgC4QFYQcpRoTFcqqM1ppX6tOJesrp1wHLYudQAKfJRUyHYqWSRkohKshPIORUSsbRPuUwu3y0jNrVuN3b1bhdjVvKbTVeQx_O7YdhRv8vclZcgS8nAKuJ54B5fRQjoA95_dOn8L_-v4wqkZ0</recordid><startdate>20060407</startdate><enddate>20060407</enddate><creator>Calonghi, Natalia</creator><creator>Pagnotta, Eleonora</creator><creator>Parolin, Carola</creator><creator>Tognoli, Cristina</creator><creator>Boga, Carla</creator><creator>Masotti, Lanfranco</creator><general>Elsevier Inc</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>7X8</scope><scope>OTOTI</scope></search><sort><creationdate>20060407</creationdate><title>9-Hydroxystearic acid interferes with EGF signalling in a human colon adenocarcinoma</title><author>Calonghi, Natalia ; Pagnotta, Eleonora ; Parolin, Carola ; Tognoli, Cristina ; Boga, Carla ; Masotti, Lanfranco</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c382t-5fce67a57191e7e96f0551945045cdb1eb664d6b4fd6a2a7137cf4a1c8ddb5783</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>60 APPLIED LIFE SCIENCES</topic><topic>9-HSA</topic><topic>Adenocarcinoma - metabolism</topic><topic>Adenocarcinoma - pathology</topic><topic>ALBUMINS</topic><topic>BLOOD SERUM</topic><topic>CARCINOMAS</topic><topic>CELL NUCLEI</topic><topic>CELL PROLIFERATION</topic><topic>Cell Proliferation - drug effects</topic><topic>Colon cancer cell</topic><topic>Colonic Neoplasms - metabolism</topic><topic>Colonic Neoplasms - pathology</topic><topic>Cyclin D1</topic><topic>Cyclin D1 - antagonists & inhibitors</topic><topic>Cyclin D1 - biosynthesis</topic><topic>Cyclin D1 - genetics</topic><topic>EGFR</topic><topic>Epidermal Growth Factor - antagonists & inhibitors</topic><topic>Epidermal Growth Factor - pharmacology</topic><topic>Epidermal Growth Factor - physiology</topic><topic>Fluorescent Antibody Technique</topic><topic>GENES</topic><topic>GROWTH FACTORS</topic><topic>HDAC1</topic><topic>Histone Deacetylase 1</topic><topic>Histone Deacetylases - metabolism</topic><topic>HT29 Cells</topic><topic>Humans</topic><topic>LARGE INTESTINE</topic><topic>Receptor, Epidermal Growth Factor - metabolism</topic><topic>RECEPTORS</topic><topic>Signal Transduction - drug effects</topic><topic>Stearic Acids - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Calonghi, Natalia</creatorcontrib><creatorcontrib>Pagnotta, Eleonora</creatorcontrib><creatorcontrib>Parolin, Carola</creatorcontrib><creatorcontrib>Tognoli, Cristina</creatorcontrib><creatorcontrib>Boga, Carla</creatorcontrib><creatorcontrib>Masotti, Lanfranco</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>OSTI.GOV</collection><jtitle>Biochemical and biophysical research communications</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Calonghi, Natalia</au><au>Pagnotta, Eleonora</au><au>Parolin, Carola</au><au>Tognoli, Cristina</au><au>Boga, Carla</au><au>Masotti, Lanfranco</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>9-Hydroxystearic acid interferes with EGF signalling in a human colon adenocarcinoma</atitle><jtitle>Biochemical and biophysical research communications</jtitle><addtitle>Biochem Biophys Res Commun</addtitle><date>2006-04-07</date><risdate>2006</risdate><volume>342</volume><issue>2</issue><spage>585</spage><epage>588</epage><pages>585-588</pages><issn>0006-291X</issn><eissn>1090-2104</eissn><abstract>The epidermal growth factor has long been known to be strictly correlated with the highly proliferating activities of cancer cells and primary tumors. Moreover, in the nucleus, the epidermal growth factor/epidermal growth factor receptor complex (EGF/EGFR) functions as a transcriptional regulator that activates the
cyclin D1 gene. 9-hydroxystearic acid (9-HSA) induces cell proliferation arrest and differentiation in HT29 colon cancer cells by inhibiting histone deacetylase 1 (HDAC1). 9-HSA-treated HT29, when stimulated with EGF, are not responsive and surprisingly undergo a further arrest. In order to understand the mechanisms of this effect, we analyzed the degree of internalization of the EGF/EGFR complex and its interactions with HDAC1. It appears that HDAC1, as modified by 9-HSA, is unable to associate with cyclin D1, interfering with the cell proliferation program, and sequesters the EGF/EGFR complex interrupting the transduction of the mitogenic signal.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>16487928</pmid><doi>10.1016/j.bbrc.2006.02.008</doi><tpages>4</tpages></addata></record> |
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subjects | 60 APPLIED LIFE SCIENCES 9-HSA Adenocarcinoma - metabolism Adenocarcinoma - pathology ALBUMINS BLOOD SERUM CARCINOMAS CELL NUCLEI CELL PROLIFERATION Cell Proliferation - drug effects Colon cancer cell Colonic Neoplasms - metabolism Colonic Neoplasms - pathology Cyclin D1 Cyclin D1 - antagonists & inhibitors Cyclin D1 - biosynthesis Cyclin D1 - genetics EGFR Epidermal Growth Factor - antagonists & inhibitors Epidermal Growth Factor - pharmacology Epidermal Growth Factor - physiology Fluorescent Antibody Technique GENES GROWTH FACTORS HDAC1 Histone Deacetylase 1 Histone Deacetylases - metabolism HT29 Cells Humans LARGE INTESTINE Receptor, Epidermal Growth Factor - metabolism RECEPTORS Signal Transduction - drug effects Stearic Acids - pharmacology |
title | 9-Hydroxystearic acid interferes with EGF signalling in a human colon adenocarcinoma |
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