Poly(ADP-ribosyl)ation of p53 induces gene-specific transcriptional repression of MTA1
The metastasis-associated protein 1 (MTA1) is overexpressed in various human cancers and is closely connected with aggressive phenotypes; however, little is known about the transcriptional regulation of the MTA1 gene. This study identified the MTA1 gene as a target of p53-mediated transrepression. T...
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| Veröffentlicht in: | Oncogene 2012-12, Vol.31 (49), p.5099-5107 |
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| description | The metastasis-associated protein 1 (MTA1) is overexpressed in various human cancers and is closely connected with aggressive phenotypes; however, little is known about the transcriptional regulation of the
MTA1
gene. This study identified the
MTA1
gene as a target of p53-mediated transrepression. The
MTA1
promoter contains two putative p53 response elements (p53REs), which were repressed by the p53-inducing drug 5-fluorouracil (5-FU). Notably, 5-FU treatment decreased
MTA1
expression only in p53 wild-type cells. p53 and histone deacetylases 1/2 were recruited, and acetylation of H3K9 was decreased on the promoter region including the p53REs after 5-FU treatment. Proteomics analysis of the p53 repressor complex, which was pulled down by the
MTA1
promoter, revealed that the poly(ADP-ribose) polymerase 1 (PARP-1) was part of the complex. Interestingly, p53 was poly(ADP-ribose)ylated by PARP-1, and the p53-mediated transrepression of the
MTA1
gene required poly(ADP-ribose)ylation of p53. In summary, we report a novel function for poly(ADP-ribose)ylation of p53 in the gene-specific regulation of the transcriptional mode of p53 on the promoter of
MTA1
. |
| doi_str_mv | 10.1038/onc.2012.2 |
| format | Article |
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MTA1
gene. This study identified the
MTA1
gene as a target of p53-mediated transrepression. The
MTA1
promoter contains two putative p53 response elements (p53REs), which were repressed by the p53-inducing drug 5-fluorouracil (5-FU). Notably, 5-FU treatment decreased
MTA1
expression only in p53 wild-type cells. p53 and histone deacetylases 1/2 were recruited, and acetylation of H3K9 was decreased on the promoter region including the p53REs after 5-FU treatment. Proteomics analysis of the p53 repressor complex, which was pulled down by the
MTA1
promoter, revealed that the poly(ADP-ribose) polymerase 1 (PARP-1) was part of the complex. Interestingly, p53 was poly(ADP-ribose)ylated by PARP-1, and the p53-mediated transrepression of the
MTA1
gene required poly(ADP-ribose)ylation of p53. In summary, we report a novel function for poly(ADP-ribose)ylation of p53 in the gene-specific regulation of the transcriptional mode of p53 on the promoter of
MTA1
.</description><identifier>ISSN: 0950-9232</identifier><identifier>EISSN: 1476-5594</identifier><identifier>DOI: 10.1038/onc.2012.2</identifier><identifier>PMID: 22286760</identifier><identifier>CODEN: ONCNES</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>5-Fluorouracil ; 631/208/200 ; 631/67 ; 631/80/458/2389 ; Acetylation ; ADP-ribosylation ; Animals ; Apoptosis ; Cancer ; Cell Biology ; Cell Line ; Drugs ; Fibroblasts - metabolism ; Fluorouracil - pharmacology ; Gene expression ; Gene Expression Regulation ; Gene regulation ; Gene silencing ; Genotype & phenotype ; Histone deacetylase ; Histone Deacetylase 1 - genetics ; Histone Deacetylase 1 - metabolism ; Histone Deacetylase 2 - genetics ; Histone Deacetylase 2 - metabolism ; Histone Deacetylases - genetics ; Histone Deacetylases - metabolism ; Histones ; Human Genetics ; Humans ; Hypoxia-Inducible Factor 1, alpha Subunit - genetics ; Hypoxia-Inducible Factor 1, alpha Subunit - metabolism ; Internal Medicine ; MCF-7 Cells - drug effects ; Medicine ; Medicine & Public Health ; Metastases ; Metastasis ; Mice ; MTA1 gene ; Oncology ; original-article ; p53 Protein ; Phenotypes ; Poly (ADP-Ribose) Polymerase-1 ; Poly Adenosine Diphosphate Ribose - metabolism ; Poly(ADP-ribose) ; Poly(ADP-ribose) polymerase ; Poly(ADP-ribose) Polymerases - genetics ; Poly(ADP-ribose) Polymerases - metabolism ; Promoter Regions, Genetic - drug effects ; Promoters ; Proteins ; Proteomics ; Regulatory sequences ; Repressor Proteins - genetics ; Repressor Proteins - metabolism ; Repressors ; Response Elements ; Ribose ; Trans-Activators ; Transcription ; Tumor Suppressor Protein p53 - genetics ; Tumor Suppressor Protein p53 - metabolism</subject><ispartof>Oncogene, 2012-12, Vol.31 (49), p.5099-5107</ispartof><rights>Macmillan Publishers Limited 2012</rights><rights>Copyright Nature Publishing Group Dec 6, 2012</rights><rights>Macmillan Publishers Limited 2012.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c448t-c9ad1f1e6822aea44b0f9e4f8791ea740d6facb0c9046b21f0f30318632a9bcf3</citedby><cites>FETCH-LOGICAL-c448t-c9ad1f1e6822aea44b0f9e4f8791ea740d6facb0c9046b21f0f30318632a9bcf3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22286760$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lee, M-H</creatorcontrib><creatorcontrib>Na, H</creatorcontrib><creatorcontrib>Kim, E-J</creatorcontrib><creatorcontrib>Lee, H-W</creatorcontrib><creatorcontrib>Lee, M-O</creatorcontrib><title>Poly(ADP-ribosyl)ation of p53 induces gene-specific transcriptional repression of MTA1</title><title>Oncogene</title><addtitle>Oncogene</addtitle><addtitle>Oncogene</addtitle><description>The metastasis-associated protein 1 (MTA1) is overexpressed in various human cancers and is closely connected with aggressive phenotypes; however, little is known about the transcriptional regulation of the
MTA1
gene. This study identified the
MTA1
gene as a target of p53-mediated transrepression. The
MTA1
promoter contains two putative p53 response elements (p53REs), which were repressed by the p53-inducing drug 5-fluorouracil (5-FU). Notably, 5-FU treatment decreased
MTA1
expression only in p53 wild-type cells. p53 and histone deacetylases 1/2 were recruited, and acetylation of H3K9 was decreased on the promoter region including the p53REs after 5-FU treatment. Proteomics analysis of the p53 repressor complex, which was pulled down by the
MTA1
promoter, revealed that the poly(ADP-ribose) polymerase 1 (PARP-1) was part of the complex. Interestingly, p53 was poly(ADP-ribose)ylated by PARP-1, and the p53-mediated transrepression of the
MTA1
gene required poly(ADP-ribose)ylation of p53. In summary, we report a novel function for poly(ADP-ribose)ylation of p53 in the gene-specific regulation of the transcriptional mode of p53 on the promoter of
MTA1
.</description><subject>5-Fluorouracil</subject><subject>631/208/200</subject><subject>631/67</subject><subject>631/80/458/2389</subject><subject>Acetylation</subject><subject>ADP-ribosylation</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Cancer</subject><subject>Cell Biology</subject><subject>Cell Line</subject><subject>Drugs</subject><subject>Fibroblasts - metabolism</subject><subject>Fluorouracil - pharmacology</subject><subject>Gene expression</subject><subject>Gene Expression Regulation</subject><subject>Gene regulation</subject><subject>Gene silencing</subject><subject>Genotype & phenotype</subject><subject>Histone deacetylase</subject><subject>Histone Deacetylase 1 - genetics</subject><subject>Histone Deacetylase 1 - metabolism</subject><subject>Histone Deacetylase 2 - genetics</subject><subject>Histone Deacetylase 2 - metabolism</subject><subject>Histone Deacetylases - genetics</subject><subject>Histone Deacetylases - metabolism</subject><subject>Histones</subject><subject>Human Genetics</subject><subject>Humans</subject><subject>Hypoxia-Inducible Factor 1, alpha Subunit - genetics</subject><subject>Hypoxia-Inducible Factor 1, alpha Subunit - metabolism</subject><subject>Internal Medicine</subject><subject>MCF-7 Cells - drug effects</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Metastases</subject><subject>Metastasis</subject><subject>Mice</subject><subject>MTA1 gene</subject><subject>Oncology</subject><subject>original-article</subject><subject>p53 Protein</subject><subject>Phenotypes</subject><subject>Poly (ADP-Ribose) Polymerase-1</subject><subject>Poly Adenosine Diphosphate Ribose - metabolism</subject><subject>Poly(ADP-ribose)</subject><subject>Poly(ADP-ribose) polymerase</subject><subject>Poly(ADP-ribose) Polymerases - genetics</subject><subject>Poly(ADP-ribose) Polymerases - metabolism</subject><subject>Promoter Regions, Genetic - drug effects</subject><subject>Promoters</subject><subject>Proteins</subject><subject>Proteomics</subject><subject>Regulatory sequences</subject><subject>Repressor Proteins - genetics</subject><subject>Repressor Proteins - metabolism</subject><subject>Repressors</subject><subject>Response Elements</subject><subject>Ribose</subject><subject>Trans-Activators</subject><subject>Transcription</subject><subject>Tumor Suppressor Protein p53 - genetics</subject><subject>Tumor Suppressor Protein p53 - metabolism</subject><issn>0950-9232</issn><issn>1476-5594</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNp90cFO3DAQBmCragUL5dIHqCL1AlRZxmPHjo8r2gISqByAq-V4xygoG6f25rBv36x2qapW4uSDP_9jzc_YJw5zDqK-iL2fI3Cc4zs241KrsqqMfM9mYCooDQo8ZEc5vwCANoAH7BARa6UVzNjTfew2p4tv92Vqm5g33Zlbt7EvYiiGShRtvxw95eKZeirzQL4NrS_WyfXZp3bYUtcViYZEOe_f3T0s-Ef2Ibgu08n-PGaPP74_XF6Xtz-vbi4Xt6WXsl6X3rglD5xUjejISdlAMCRDrQ0npyUsVXC-AW9AqgZ5gCBA8FoJdKbxQRyz013ukOKvkfLartrsqetcT3HMlmOlta61FhP98g99iWOavp8tKskr0ILrtxSftiYAFTeTOt8pn2LOiYIdUrtyaWM52G0ndurEbjuxOOHP-8ixWdHyD30tYQJfdyBPV_0zpb9m_h_3G64kk6Y</recordid><startdate>20121206</startdate><enddate>20121206</enddate><creator>Lee, M-H</creator><creator>Na, H</creator><creator>Kim, E-J</creator><creator>Lee, H-W</creator><creator>Lee, M-O</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></search><sort><creationdate>20121206</creationdate><title>Poly(ADP-ribosyl)ation of p53 induces gene-specific transcriptional repression of MTA1</title><author>Lee, M-H ; Na, H ; Kim, E-J ; Lee, H-W ; Lee, M-O</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c448t-c9ad1f1e6822aea44b0f9e4f8791ea740d6facb0c9046b21f0f30318632a9bcf3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>5-Fluorouracil</topic><topic>631/208/200</topic><topic>631/67</topic><topic>631/80/458/2389</topic><topic>Acetylation</topic><topic>ADP-ribosylation</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Cancer</topic><topic>Cell Biology</topic><topic>Cell Line</topic><topic>Drugs</topic><topic>Fibroblasts - metabolism</topic><topic>Fluorouracil - pharmacology</topic><topic>Gene expression</topic><topic>Gene Expression Regulation</topic><topic>Gene regulation</topic><topic>Gene silencing</topic><topic>Genotype & phenotype</topic><topic>Histone deacetylase</topic><topic>Histone Deacetylase 1 - genetics</topic><topic>Histone Deacetylase 1 - metabolism</topic><topic>Histone Deacetylase 2 - genetics</topic><topic>Histone Deacetylase 2 - metabolism</topic><topic>Histone Deacetylases - genetics</topic><topic>Histone Deacetylases - metabolism</topic><topic>Histones</topic><topic>Human Genetics</topic><topic>Humans</topic><topic>Hypoxia-Inducible Factor 1, alpha Subunit - genetics</topic><topic>Hypoxia-Inducible Factor 1, alpha Subunit - metabolism</topic><topic>Internal Medicine</topic><topic>MCF-7 Cells - drug effects</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Metastases</topic><topic>Metastasis</topic><topic>Mice</topic><topic>MTA1 gene</topic><topic>Oncology</topic><topic>original-article</topic><topic>p53 Protein</topic><topic>Phenotypes</topic><topic>Poly (ADP-Ribose) Polymerase-1</topic><topic>Poly Adenosine Diphosphate Ribose - metabolism</topic><topic>Poly(ADP-ribose)</topic><topic>Poly(ADP-ribose) polymerase</topic><topic>Poly(ADP-ribose) Polymerases - genetics</topic><topic>Poly(ADP-ribose) Polymerases - metabolism</topic><topic>Promoter Regions, Genetic - drug effects</topic><topic>Promoters</topic><topic>Proteins</topic><topic>Proteomics</topic><topic>Regulatory sequences</topic><topic>Repressor Proteins - genetics</topic><topic>Repressor Proteins - metabolism</topic><topic>Repressors</topic><topic>Response Elements</topic><topic>Ribose</topic><topic>Trans-Activators</topic><topic>Transcription</topic><topic>Tumor Suppressor Protein p53 - genetics</topic><topic>Tumor Suppressor Protein p53 - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lee, M-H</creatorcontrib><creatorcontrib>Na, H</creatorcontrib><creatorcontrib>Kim, E-J</creatorcontrib><creatorcontrib>Lee, H-W</creatorcontrib><creatorcontrib>Lee, M-O</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><jtitle>Oncogene</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lee, M-H</au><au>Na, H</au><au>Kim, E-J</au><au>Lee, H-W</au><au>Lee, M-O</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Poly(ADP-ribosyl)ation of p53 induces gene-specific transcriptional repression of MTA1</atitle><jtitle>Oncogene</jtitle><stitle>Oncogene</stitle><addtitle>Oncogene</addtitle><date>2012-12-06</date><risdate>2012</risdate><volume>31</volume><issue>49</issue><spage>5099</spage><epage>5107</epage><pages>5099-5107</pages><issn>0950-9232</issn><eissn>1476-5594</eissn><coden>ONCNES</coden><abstract>The metastasis-associated protein 1 (MTA1) is overexpressed in various human cancers and is closely connected with aggressive phenotypes; however, little is known about the transcriptional regulation of the
MTA1
gene. This study identified the
MTA1
gene as a target of p53-mediated transrepression. The
MTA1
promoter contains two putative p53 response elements (p53REs), which were repressed by the p53-inducing drug 5-fluorouracil (5-FU). Notably, 5-FU treatment decreased
MTA1
expression only in p53 wild-type cells. p53 and histone deacetylases 1/2 were recruited, and acetylation of H3K9 was decreased on the promoter region including the p53REs after 5-FU treatment. Proteomics analysis of the p53 repressor complex, which was pulled down by the
MTA1
promoter, revealed that the poly(ADP-ribose) polymerase 1 (PARP-1) was part of the complex. Interestingly, p53 was poly(ADP-ribose)ylated by PARP-1, and the p53-mediated transrepression of the
MTA1
gene required poly(ADP-ribose)ylation of p53. In summary, we report a novel function for poly(ADP-ribose)ylation of p53 in the gene-specific regulation of the transcriptional mode of p53 on the promoter of
MTA1
.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>22286760</pmid><doi>10.1038/onc.2012.2</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; Nature; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection |
| subjects | 5-Fluorouracil 631/208/200 631/67 631/80/458/2389 Acetylation ADP-ribosylation Animals Apoptosis Cancer Cell Biology Cell Line Drugs Fibroblasts - metabolism Fluorouracil - pharmacology Gene expression Gene Expression Regulation Gene regulation Gene silencing Genotype & phenotype Histone deacetylase Histone Deacetylase 1 - genetics Histone Deacetylase 1 - metabolism Histone Deacetylase 2 - genetics Histone Deacetylase 2 - metabolism Histone Deacetylases - genetics Histone Deacetylases - metabolism Histones Human Genetics Humans Hypoxia-Inducible Factor 1, alpha Subunit - genetics Hypoxia-Inducible Factor 1, alpha Subunit - metabolism Internal Medicine MCF-7 Cells - drug effects Medicine Medicine & Public Health Metastases Metastasis Mice MTA1 gene Oncology original-article p53 Protein Phenotypes Poly (ADP-Ribose) Polymerase-1 Poly Adenosine Diphosphate Ribose - metabolism Poly(ADP-ribose) Poly(ADP-ribose) polymerase Poly(ADP-ribose) Polymerases - genetics Poly(ADP-ribose) Polymerases - metabolism Promoter Regions, Genetic - drug effects Promoters Proteins Proteomics Regulatory sequences Repressor Proteins - genetics Repressor Proteins - metabolism Repressors Response Elements Ribose Trans-Activators Transcription Tumor Suppressor Protein p53 - genetics Tumor Suppressor Protein p53 - metabolism |
| title | Poly(ADP-ribosyl)ation of p53 induces gene-specific transcriptional repression of MTA1 |
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