Mutant p53 gains new function in promoting inflammatory signals by repression of the secreted interleukin-1 receptor antagonist
The TP53 tumor-suppressor gene is frequently mutated in human cancer. Missense mutations can add novel functions (gain-of-function, GOF) that promote tumor malignancy. Here we report that mutant (mut) p53 promotes tumor malignancy by suppressing the expression of a natural occurring anti-inflammator...
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| Veröffentlicht in: | Oncogene 2015-05, Vol.34 (19), p.2493-2504 |
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| creator | Ubertini, V Norelli, G D'Arcangelo, D Gurtner, A Cesareo, E Baldari, S Gentileschi, M P Piaggio, G Nisticò, P Soddu, S Facchiano, A Bossi, G |
| description | The
TP53
tumor-suppressor gene is frequently mutated in human cancer. Missense mutations can add novel functions (gain-of-function, GOF) that promote tumor malignancy. Here we report that mutant (mut) p53 promotes tumor malignancy by suppressing the expression of a natural occurring anti-inflammatory cytokine, the secreted interleukin-1 receptor antagonist (sIL-1Ra, IL1RN). We show that mutp53 but not wild-type (wt) p53 suppresses the sIL-1Ra production in conditioned media of cancer cells. Moreover, mutp53, but not wtp53, binds physically the sIL-1Ra promoter and the protein–protein interaction with the transcriptional co-repressor MAFF (v-MAF musculoaponeurotic fibrosarcoma oncogene family, protein F) is required for mutp53-induced sIL-1Ra suppression. Remarkably, when exposed to IL-1 beta (IL-1β) inflammatory stimuli, mutp53 sustains a ready-to-be-activated
in vitro
and
in vivo
cancer cells’ response through the sIL-1Ra repression. Taken together, these results identify sIL-1Ra as a novel mutp53 target gene, whose suppression might be required to generate a chronic pro-inflammatory tumor microenvironment through which mutp53 promotes tumor malignancy. |
| doi_str_mv | 10.1038/onc.2014.191 |
| format | Article |
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TP53
tumor-suppressor gene is frequently mutated in human cancer. Missense mutations can add novel functions (gain-of-function, GOF) that promote tumor malignancy. Here we report that mutant (mut) p53 promotes tumor malignancy by suppressing the expression of a natural occurring anti-inflammatory cytokine, the secreted interleukin-1 receptor antagonist (sIL-1Ra, IL1RN). We show that mutp53 but not wild-type (wt) p53 suppresses the sIL-1Ra production in conditioned media of cancer cells. Moreover, mutp53, but not wtp53, binds physically the sIL-1Ra promoter and the protein–protein interaction with the transcriptional co-repressor MAFF (v-MAF musculoaponeurotic fibrosarcoma oncogene family, protein F) is required for mutp53-induced sIL-1Ra suppression. Remarkably, when exposed to IL-1 beta (IL-1β) inflammatory stimuli, mutp53 sustains a ready-to-be-activated
in vitro
and
in vivo
cancer cells’ response through the sIL-1Ra repression. Taken together, these results identify sIL-1Ra as a novel mutp53 target gene, whose suppression might be required to generate a chronic pro-inflammatory tumor microenvironment through which mutp53 promotes tumor malignancy.</description><identifier>ISSN: 0950-9232</identifier><identifier>EISSN: 1476-5594</identifier><identifier>DOI: 10.1038/onc.2014.191</identifier><identifier>PMID: 24998848</identifier><identifier>CODEN: ONCNES</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>101/1 ; 38/109 ; 38/77 ; 38/89 ; 42/44 ; 631/250/256 ; 631/67 ; 631/67/327 ; 631/80/86 ; 64/60 ; 82/29 ; 82/80 ; 96/106 ; 96/21 ; Analysis ; Apoptosis ; Cancer ; Cancer cells ; Care and treatment ; Cell Biology ; Cell Line, Tumor ; Cell proliferation ; Chemotherapy ; Cytokines ; DNA-Binding Proteins - genetics ; Fibrosarcoma ; Gene expression ; Health aspects ; Hep G2 Cells ; HT29 Cells ; Human Genetics ; Humans ; IL-1β ; Inflammation ; Inflammation - genetics ; Inflammation - immunology ; Interleukin 1 ; Interleukin 1 receptor antagonist ; Interleukin 1 Receptor Antagonist Protein - antagonists & inhibitors ; Interleukin 1 Receptor Antagonist Protein - biosynthesis ; Interleukin 1 Receptor Antagonist Protein - genetics ; Interleukin-1beta - pharmacology ; Internal Medicine ; MafF Transcription Factor - metabolism ; Malignancy ; MCF-7 Cells ; Medicine ; Medicine & Public Health ; Missense mutation ; Mutants ; Mutation ; Neoplasms - genetics ; Neoplasms - mortality ; Nuclear Proteins - metabolism ; Oncology ; original-article ; p53 Protein ; Prognosis ; Promoter Regions, Genetic - genetics ; Protein Binding ; Proteins ; RNA Interference ; RNA, Small Interfering ; Transcription ; Tumor Microenvironment - immunology ; Tumor Suppressor Protein p53 - genetics ; Tumors</subject><ispartof>Oncogene, 2015-05, Vol.34 (19), p.2493-2504</ispartof><rights>Macmillan Publishers Limited 2015</rights><rights>COPYRIGHT 2015 Nature Publishing Group</rights><rights>Copyright Nature Publishing Group May 7, 2015</rights><rights>Macmillan Publishers Limited 2015.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c659t-4d435abdc74ce25607141fa0c8baccac931a4c7d3bb6117d6fbd0d280db7b8903</citedby><cites>FETCH-LOGICAL-c659t-4d435abdc74ce25607141fa0c8baccac931a4c7d3bb6117d6fbd0d280db7b8903</cites><orcidid>0000-0003-2114-1892 ; 0000000321141892</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1038/onc.2014.191$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/onc.2014.191$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24998848$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ubertini, V</creatorcontrib><creatorcontrib>Norelli, G</creatorcontrib><creatorcontrib>D'Arcangelo, D</creatorcontrib><creatorcontrib>Gurtner, A</creatorcontrib><creatorcontrib>Cesareo, E</creatorcontrib><creatorcontrib>Baldari, S</creatorcontrib><creatorcontrib>Gentileschi, M P</creatorcontrib><creatorcontrib>Piaggio, G</creatorcontrib><creatorcontrib>Nisticò, P</creatorcontrib><creatorcontrib>Soddu, S</creatorcontrib><creatorcontrib>Facchiano, A</creatorcontrib><creatorcontrib>Bossi, G</creatorcontrib><title>Mutant p53 gains new function in promoting inflammatory signals by repression of the secreted interleukin-1 receptor antagonist</title><title>Oncogene</title><addtitle>Oncogene</addtitle><addtitle>Oncogene</addtitle><description>The
TP53
tumor-suppressor gene is frequently mutated in human cancer. Missense mutations can add novel functions (gain-of-function, GOF) that promote tumor malignancy. Here we report that mutant (mut) p53 promotes tumor malignancy by suppressing the expression of a natural occurring anti-inflammatory cytokine, the secreted interleukin-1 receptor antagonist (sIL-1Ra, IL1RN). We show that mutp53 but not wild-type (wt) p53 suppresses the sIL-1Ra production in conditioned media of cancer cells. Moreover, mutp53, but not wtp53, binds physically the sIL-1Ra promoter and the protein–protein interaction with the transcriptional co-repressor MAFF (v-MAF musculoaponeurotic fibrosarcoma oncogene family, protein F) is required for mutp53-induced sIL-1Ra suppression. Remarkably, when exposed to IL-1 beta (IL-1β) inflammatory stimuli, mutp53 sustains a ready-to-be-activated
in vitro
and
in vivo
cancer cells’ response through the sIL-1Ra repression. Taken together, these results identify sIL-1Ra as a novel mutp53 target gene, whose suppression might be required to generate a chronic pro-inflammatory tumor microenvironment through which mutp53 promotes tumor malignancy.</description><subject>101/1</subject><subject>38/109</subject><subject>38/77</subject><subject>38/89</subject><subject>42/44</subject><subject>631/250/256</subject><subject>631/67</subject><subject>631/67/327</subject><subject>631/80/86</subject><subject>64/60</subject><subject>82/29</subject><subject>82/80</subject><subject>96/106</subject><subject>96/21</subject><subject>Analysis</subject><subject>Apoptosis</subject><subject>Cancer</subject><subject>Cancer cells</subject><subject>Care and treatment</subject><subject>Cell Biology</subject><subject>Cell Line, Tumor</subject><subject>Cell proliferation</subject><subject>Chemotherapy</subject><subject>Cytokines</subject><subject>DNA-Binding Proteins - genetics</subject><subject>Fibrosarcoma</subject><subject>Gene expression</subject><subject>Health aspects</subject><subject>Hep G2 Cells</subject><subject>HT29 Cells</subject><subject>Human Genetics</subject><subject>Humans</subject><subject>IL-1β</subject><subject>Inflammation</subject><subject>Inflammation - genetics</subject><subject>Inflammation - immunology</subject><subject>Interleukin 1</subject><subject>Interleukin 1 receptor antagonist</subject><subject>Interleukin 1 Receptor Antagonist Protein - antagonists & inhibitors</subject><subject>Interleukin 1 Receptor Antagonist Protein - biosynthesis</subject><subject>Interleukin 1 Receptor Antagonist Protein - genetics</subject><subject>Interleukin-1beta - pharmacology</subject><subject>Internal Medicine</subject><subject>MafF Transcription Factor - metabolism</subject><subject>Malignancy</subject><subject>MCF-7 Cells</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Missense mutation</subject><subject>Mutants</subject><subject>Mutation</subject><subject>Neoplasms - genetics</subject><subject>Neoplasms - mortality</subject><subject>Nuclear Proteins - metabolism</subject><subject>Oncology</subject><subject>original-article</subject><subject>p53 Protein</subject><subject>Prognosis</subject><subject>Promoter Regions, Genetic - genetics</subject><subject>Protein Binding</subject><subject>Proteins</subject><subject>RNA Interference</subject><subject>RNA, Small Interfering</subject><subject>Transcription</subject><subject>Tumor Microenvironment - immunology</subject><subject>Tumor Suppressor Protein p53 - genetics</subject><subject>Tumors</subject><issn>0950-9232</issn><issn>1476-5594</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNqNksuP1SAUxhujca6jO9eGxI0Le-XVAsvJxFcyxo2uCYXTytjCFWjMXfmvS3PHZybGsCDA7_sO5-RrmscE7wlm8kUMdk8x4XuiyJ1mR7jo265T_G6zw6rDraKMnjUPcr7GGAuF6f3mjHKlpORy13x7txYTCjp0DE3Gh4wCfEXjGmzxMSAf0CHFJRYfpnoYZ7MspsR0RNlPwcwZDUeU4JAg542PIyqfAGWwCQq4KimQZlg_-9CSClo4VDWqFc0Ug8_lYXNvrDbw6GY_bz6-evnh8k179f7128uLq9b2nSotd5x1ZnBWcAu067EgnIwGWzkYa41VjBhuhWPD0BMiXD8ODjsqsRvEIBVm582zk29t58sKuejFZwvzbALENWvSS8Y6Qf4PxUTIHpOKPv0LvY5r2uaiKWOkJ5Wk_6JILxSlnRTiFzWZGXSddSzJ2K20vuCES8oZ55Xa30LV5WDxNgYYfb3_Q_D8JLAp5pxg1IfkF5OOmmC9BUjXAOktQLoGqOJPbv66Dgu4n_CPxFSgPQG5PoUJ0m_N3Gb4Ha4xzyk</recordid><startdate>20150507</startdate><enddate>20150507</enddate><creator>Ubertini, V</creator><creator>Norelli, G</creator><creator>D'Arcangelo, D</creator><creator>Gurtner, A</creator><creator>Cesareo, E</creator><creator>Baldari, S</creator><creator>Gentileschi, M P</creator><creator>Piaggio, G</creator><creator>Nisticò, P</creator><creator>Soddu, S</creator><creator>Facchiano, A</creator><creator>Bossi, G</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</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>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>M7P</scope><scope>MBDVC</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>RC3</scope><scope>7X8</scope><scope>7T5</scope><orcidid>https://orcid.org/0000-0003-2114-1892</orcidid><orcidid>https://orcid.org/0000000321141892</orcidid></search><sort><creationdate>20150507</creationdate><title>Mutant p53 gains new function in promoting inflammatory signals by repression of the secreted interleukin-1 receptor antagonist</title><author>Ubertini, V ; Norelli, G ; D'Arcangelo, D ; Gurtner, A ; Cesareo, E ; Baldari, S ; Gentileschi, M P ; Piaggio, G ; Nisticò, P ; Soddu, S ; Facchiano, A ; Bossi, G</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c659t-4d435abdc74ce25607141fa0c8baccac931a4c7d3bb6117d6fbd0d280db7b8903</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>101/1</topic><topic>38/109</topic><topic>38/77</topic><topic>38/89</topic><topic>42/44</topic><topic>631/250/256</topic><topic>631/67</topic><topic>631/67/327</topic><topic>631/80/86</topic><topic>64/60</topic><topic>82/29</topic><topic>82/80</topic><topic>96/106</topic><topic>96/21</topic><topic>Analysis</topic><topic>Apoptosis</topic><topic>Cancer</topic><topic>Cancer cells</topic><topic>Care and treatment</topic><topic>Cell Biology</topic><topic>Cell Line, Tumor</topic><topic>Cell proliferation</topic><topic>Chemotherapy</topic><topic>Cytokines</topic><topic>DNA-Binding Proteins - genetics</topic><topic>Fibrosarcoma</topic><topic>Gene expression</topic><topic>Health aspects</topic><topic>Hep G2 Cells</topic><topic>HT29 Cells</topic><topic>Human Genetics</topic><topic>Humans</topic><topic>IL-1β</topic><topic>Inflammation</topic><topic>Inflammation - genetics</topic><topic>Inflammation - immunology</topic><topic>Interleukin 1</topic><topic>Interleukin 1 receptor antagonist</topic><topic>Interleukin 1 Receptor Antagonist Protein - antagonists & inhibitors</topic><topic>Interleukin 1 Receptor Antagonist Protein - biosynthesis</topic><topic>Interleukin 1 Receptor Antagonist Protein - genetics</topic><topic>Interleukin-1beta - pharmacology</topic><topic>Internal Medicine</topic><topic>MafF Transcription Factor - metabolism</topic><topic>Malignancy</topic><topic>MCF-7 Cells</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Missense mutation</topic><topic>Mutants</topic><topic>Mutation</topic><topic>Neoplasms - genetics</topic><topic>Neoplasms - mortality</topic><topic>Nuclear Proteins - metabolism</topic><topic>Oncology</topic><topic>original-article</topic><topic>p53 Protein</topic><topic>Prognosis</topic><topic>Promoter Regions, Genetic - genetics</topic><topic>Protein Binding</topic><topic>Proteins</topic><topic>RNA Interference</topic><topic>RNA, Small Interfering</topic><topic>Transcription</topic><topic>Tumor Microenvironment - immunology</topic><topic>Tumor Suppressor Protein p53 - genetics</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ubertini, V</creatorcontrib><creatorcontrib>Norelli, G</creatorcontrib><creatorcontrib>D'Arcangelo, D</creatorcontrib><creatorcontrib>Gurtner, A</creatorcontrib><creatorcontrib>Cesareo, E</creatorcontrib><creatorcontrib>Baldari, S</creatorcontrib><creatorcontrib>Gentileschi, M P</creatorcontrib><creatorcontrib>Piaggio, G</creatorcontrib><creatorcontrib>Nisticò, P</creatorcontrib><creatorcontrib>Soddu, S</creatorcontrib><creatorcontrib>Facchiano, A</creatorcontrib><creatorcontrib>Bossi, G</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>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</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>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</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>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Biological Science Database</collection><collection>Research Library (Corporate)</collection><collection>Biotechnology and BioEngineering Abstracts</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><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>Immunology Abstracts</collection><jtitle>Oncogene</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ubertini, V</au><au>Norelli, G</au><au>D'Arcangelo, D</au><au>Gurtner, A</au><au>Cesareo, E</au><au>Baldari, S</au><au>Gentileschi, M P</au><au>Piaggio, G</au><au>Nisticò, P</au><au>Soddu, S</au><au>Facchiano, A</au><au>Bossi, G</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Mutant p53 gains new function in promoting inflammatory signals by repression of the secreted interleukin-1 receptor antagonist</atitle><jtitle>Oncogene</jtitle><stitle>Oncogene</stitle><addtitle>Oncogene</addtitle><date>2015-05-07</date><risdate>2015</risdate><volume>34</volume><issue>19</issue><spage>2493</spage><epage>2504</epage><pages>2493-2504</pages><issn>0950-9232</issn><eissn>1476-5594</eissn><coden>ONCNES</coden><abstract>The
TP53
tumor-suppressor gene is frequently mutated in human cancer. Missense mutations can add novel functions (gain-of-function, GOF) that promote tumor malignancy. Here we report that mutant (mut) p53 promotes tumor malignancy by suppressing the expression of a natural occurring anti-inflammatory cytokine, the secreted interleukin-1 receptor antagonist (sIL-1Ra, IL1RN). We show that mutp53 but not wild-type (wt) p53 suppresses the sIL-1Ra production in conditioned media of cancer cells. Moreover, mutp53, but not wtp53, binds physically the sIL-1Ra promoter and the protein–protein interaction with the transcriptional co-repressor MAFF (v-MAF musculoaponeurotic fibrosarcoma oncogene family, protein F) is required for mutp53-induced sIL-1Ra suppression. Remarkably, when exposed to IL-1 beta (IL-1β) inflammatory stimuli, mutp53 sustains a ready-to-be-activated
in vitro
and
in vivo
cancer cells’ response through the sIL-1Ra repression. Taken together, these results identify sIL-1Ra as a novel mutp53 target gene, whose suppression might be required to generate a chronic pro-inflammatory tumor microenvironment through which mutp53 promotes tumor malignancy.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>24998848</pmid><doi>10.1038/onc.2014.191</doi><tpages>12</tpages><orcidid>https://orcid.org/0000-0003-2114-1892</orcidid><orcidid>https://orcid.org/0000000321141892</orcidid><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0950-9232 |
| ispartof | Oncogene, 2015-05, Vol.34 (19), p.2493-2504 |
| issn | 0950-9232 1476-5594 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_1683357190 |
| source | MEDLINE; Nature Journals Online; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; SpringerLink Journals - AutoHoldings |
| subjects | 101/1 38/109 38/77 38/89 42/44 631/250/256 631/67 631/67/327 631/80/86 64/60 82/29 82/80 96/106 96/21 Analysis Apoptosis Cancer Cancer cells Care and treatment Cell Biology Cell Line, Tumor Cell proliferation Chemotherapy Cytokines DNA-Binding Proteins - genetics Fibrosarcoma Gene expression Health aspects Hep G2 Cells HT29 Cells Human Genetics Humans IL-1β Inflammation Inflammation - genetics Inflammation - immunology Interleukin 1 Interleukin 1 receptor antagonist Interleukin 1 Receptor Antagonist Protein - antagonists & inhibitors Interleukin 1 Receptor Antagonist Protein - biosynthesis Interleukin 1 Receptor Antagonist Protein - genetics Interleukin-1beta - pharmacology Internal Medicine MafF Transcription Factor - metabolism Malignancy MCF-7 Cells Medicine Medicine & Public Health Missense mutation Mutants Mutation Neoplasms - genetics Neoplasms - mortality Nuclear Proteins - metabolism Oncology original-article p53 Protein Prognosis Promoter Regions, Genetic - genetics Protein Binding Proteins RNA Interference RNA, Small Interfering Transcription Tumor Microenvironment - immunology Tumor Suppressor Protein p53 - genetics Tumors |
| title | Mutant p53 gains new function in promoting inflammatory signals by repression of the secreted interleukin-1 receptor antagonist |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-08T05%3A15%3A52IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_proqu&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Mutant%20p53%20gains%20new%20function%20in%20promoting%20inflammatory%20signals%20by%20repression%20of%20the%20secreted%20interleukin-1%20receptor%20antagonist&rft.jtitle=Oncogene&rft.au=Ubertini,%20V&rft.date=2015-05-07&rft.volume=34&rft.issue=19&rft.spage=2493&rft.epage=2504&rft.pages=2493-2504&rft.issn=0950-9232&rft.eissn=1476-5594&rft.coden=ONCNES&rft_id=info:doi/10.1038/onc.2014.191&rft_dat=%3Cgale_proqu%3EA414824344%3C/gale_proqu%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1679225877&rft_id=info:pmid/24998848&rft_galeid=A414824344&rfr_iscdi=true |