Histone acetylation and steroid receptor coactivator expression during clofibrate‐induced rat hepatocarcinogenesis
Peroxisome proliferators (PPs), non‐genotoxic rodent carcinogens, cause the induction of the peroxisomal fatty acid β‐oxidation system, including bifunctional enzyme (BE) and 3‐ketoacyl‐CoA thiolase (TH), in the liver. GST M1 gene is polymorphic in Sprague–Dawley rats, NC‐ and KS‐type. The KS‐type r...
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| creator | Asano, Jumpei Kudo, Toshihiro Shimizu, Takeshi Fan, Yang Nanashima, Naoki Yamana, Daisuke Miura, Takuya Yamada, Toshiyuki Tsuchida, Shigeki |
| description | Peroxisome proliferators (PPs), non‐genotoxic rodent carcinogens, cause the induction of the peroxisomal fatty acid β‐oxidation system, including bifunctional enzyme (BE) and 3‐ketoacyl‐CoA thiolase (TH), in the liver. GST M1 gene is polymorphic in Sprague–Dawley rats, NC‐ and KS‐type. The KS‐type rats showed enhanced susceptibility to ethyl‐α‐chlorophenoxyisobutyrate (clofibrate, CF), one of the PPs. The degree of BE induction was higher in the KS‐type and preneoplastic foci developed after 6–8 weeks of treatment, whereas no foci developed in the NC‐type. In the preset study, factors involved in different BE inducibility were investigated. There were no differences in hepatic peroxisome proliferator‐activated receptor (PPAR) α levels between them. Among various coactivators for PPARα, only steroid receptor coactivator (SRC)‐3 level was higher in the KS‐type. To investigate the association between PPARα and SRC‐3 or other proteins, nuclear extracts from CF‐treated livers were applied to a PPARα column. In the KS‐type, 110, 72, and 42 kDa proteins were bound and these were identified as SRC‐3, BE, and TH, respectively. EMSA supported the binding of these proteins to PPARα associated to the BE enhancer in CF‐treated KS‐type, but not in the NC‐type. Histone H3 acetylation was increased 11‐fold in the KS‐type by CF treatment but not in the NC‐type. As BE and TH are responsible for acetyl‐CoA production and SRC‐3 possesses a histone acetyltransferase activity, these results suggest that enhanced BE induction in the KS‐type livers is due to acetylation‐mediated transcriptional activation and epigenetic mechanisms might be involved in CF‐induced rat hepatocarcinogenesis.
(Cancer Sci 2010; 101: 876–875) |
| doi_str_mv | 10.1111/j.1349-7006.2009.01460.x |
| format | Article |
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(Cancer Sci 2010; 101: 876–875)</description><identifier>ISSN: 1347-9032</identifier><identifier>ISSN: 1349-7006</identifier><identifier>EISSN: 1349-7006</identifier><identifier>DOI: 10.1111/j.1349-7006.2009.01460.x</identifier><identifier>PMID: 20132223</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Acetyl Coenzyme A - genetics ; Acetyl Coenzyme A - metabolism ; Acetyl Coenzyme A - pharmacology ; Acetyl-CoA C-Acetyltransferase - genetics ; Acetyl-CoA C-Acetyltransferase - metabolism ; Acetylation ; Animals ; Antibodies ; Biological and medical sciences ; Carcinogens ; Cell Transformation, Neoplastic - genetics ; Cell Transformation, Neoplastic - metabolism ; Clofibrate ; Enzyme Induction ; Enzymes ; Epigenetics ; Fatty acids ; Fatty Acids - genetics ; Fatty Acids - metabolism ; Fatty Acids - pharmacology ; Gastroenterology. Liver. Pancreas. Abdomen ; Genes ; Genotoxicity ; Histone acetyltransferase ; Histone H3 ; Histones - genetics ; Histones - metabolism ; Histones - pharmacology ; Liver ; Liver - drug effects ; Liver - enzymology ; Liver - metabolism ; Liver Neoplasms, Experimental - chemically induced ; Liver Neoplasms, Experimental - metabolism ; Liver. Biliary tract. Portal circulation. Exocrine pancreas ; Male ; Medical sciences ; Nuclear Receptor Coactivator 3 - metabolism ; Original ; Oxidation ; Peptides ; Peroxisome proliferator-activated receptors ; Peroxisome Proliferators - metabolism ; Peroxisome Proliferators - pharmacology ; Polymorphism, Genetic ; PPAR alpha - genetics ; PPAR alpha - metabolism ; PPAR alpha - pharmacology ; Proteins ; Rats ; Rats, Sprague-Dawley ; Receptors, Steroid - genetics ; Receptors, Steroid - metabolism ; Steroids ; Thiolase ; Transcription activation ; Tumors</subject><ispartof>Cancer science, 2010-04, Vol.101 (4), p.869-875</ispartof><rights>2010 Japanese Cancer Association</rights><rights>2015 INIST-CNRS</rights><rights>Copyright John Wiley & Sons, Inc. Apr 2010</rights><rights>Copyright John Wiley & Sons, Inc. 2010</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c7430-fa083fba47512cf99bba0213eab1a9b9cd9fe9c627a0096d1e40aa645ccfbb923</citedby><cites>FETCH-LOGICAL-c7430-fa083fba47512cf99bba0213eab1a9b9cd9fe9c627a0096d1e40aa645ccfbb923</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC11158118/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC11158118/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,725,778,782,883,1414,11545,27907,27908,45557,45558,46035,46459,53774,53776</link.rule.ids><linktorsrc>$$Uhttps://onlinelibrary.wiley.com/doi/abs/10.1111%2Fj.1349-7006.2009.01460.x$$EView_record_in_Wiley-Blackwell$$FView_record_in_$$GWiley-Blackwell</linktorsrc><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=22963631$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20132223$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Asano, Jumpei</creatorcontrib><creatorcontrib>Kudo, Toshihiro</creatorcontrib><creatorcontrib>Shimizu, Takeshi</creatorcontrib><creatorcontrib>Fan, Yang</creatorcontrib><creatorcontrib>Nanashima, Naoki</creatorcontrib><creatorcontrib>Yamana, Daisuke</creatorcontrib><creatorcontrib>Miura, Takuya</creatorcontrib><creatorcontrib>Yamada, Toshiyuki</creatorcontrib><creatorcontrib>Tsuchida, Shigeki</creatorcontrib><title>Histone acetylation and steroid receptor coactivator expression during clofibrate‐induced rat hepatocarcinogenesis</title><title>Cancer science</title><addtitle>Cancer Sci</addtitle><description>Peroxisome proliferators (PPs), non‐genotoxic rodent carcinogens, cause the induction of the peroxisomal fatty acid β‐oxidation system, including bifunctional enzyme (BE) and 3‐ketoacyl‐CoA thiolase (TH), in the liver. GST M1 gene is polymorphic in Sprague–Dawley rats, NC‐ and KS‐type. The KS‐type rats showed enhanced susceptibility to ethyl‐α‐chlorophenoxyisobutyrate (clofibrate, CF), one of the PPs. The degree of BE induction was higher in the KS‐type and preneoplastic foci developed after 6–8 weeks of treatment, whereas no foci developed in the NC‐type. In the preset study, factors involved in different BE inducibility were investigated. There were no differences in hepatic peroxisome proliferator‐activated receptor (PPAR) α levels between them. Among various coactivators for PPARα, only steroid receptor coactivator (SRC)‐3 level was higher in the KS‐type. To investigate the association between PPARα and SRC‐3 or other proteins, nuclear extracts from CF‐treated livers were applied to a PPARα column. In the KS‐type, 110, 72, and 42 kDa proteins were bound and these were identified as SRC‐3, BE, and TH, respectively. EMSA supported the binding of these proteins to PPARα associated to the BE enhancer in CF‐treated KS‐type, but not in the NC‐type. Histone H3 acetylation was increased 11‐fold in the KS‐type by CF treatment but not in the NC‐type. As BE and TH are responsible for acetyl‐CoA production and SRC‐3 possesses a histone acetyltransferase activity, these results suggest that enhanced BE induction in the KS‐type livers is due to acetylation‐mediated transcriptional activation and epigenetic mechanisms might be involved in CF‐induced rat hepatocarcinogenesis.
(Cancer Sci 2010; 101: 876–875)</description><subject>Acetyl Coenzyme A - genetics</subject><subject>Acetyl Coenzyme A - metabolism</subject><subject>Acetyl Coenzyme A - pharmacology</subject><subject>Acetyl-CoA C-Acetyltransferase - genetics</subject><subject>Acetyl-CoA C-Acetyltransferase - metabolism</subject><subject>Acetylation</subject><subject>Animals</subject><subject>Antibodies</subject><subject>Biological and medical sciences</subject><subject>Carcinogens</subject><subject>Cell Transformation, Neoplastic - genetics</subject><subject>Cell Transformation, Neoplastic - metabolism</subject><subject>Clofibrate</subject><subject>Enzyme Induction</subject><subject>Enzymes</subject><subject>Epigenetics</subject><subject>Fatty acids</subject><subject>Fatty Acids - genetics</subject><subject>Fatty Acids - metabolism</subject><subject>Fatty Acids - pharmacology</subject><subject>Gastroenterology. Liver. Pancreas. Abdomen</subject><subject>Genes</subject><subject>Genotoxicity</subject><subject>Histone acetyltransferase</subject><subject>Histone H3</subject><subject>Histones - genetics</subject><subject>Histones - metabolism</subject><subject>Histones - pharmacology</subject><subject>Liver</subject><subject>Liver - drug effects</subject><subject>Liver - enzymology</subject><subject>Liver - metabolism</subject><subject>Liver Neoplasms, Experimental - chemically induced</subject><subject>Liver Neoplasms, Experimental - metabolism</subject><subject>Liver. Biliary tract. Portal circulation. Exocrine pancreas</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Nuclear Receptor Coactivator 3 - metabolism</subject><subject>Original</subject><subject>Oxidation</subject><subject>Peptides</subject><subject>Peroxisome proliferator-activated receptors</subject><subject>Peroxisome Proliferators - metabolism</subject><subject>Peroxisome Proliferators - pharmacology</subject><subject>Polymorphism, Genetic</subject><subject>PPAR alpha - genetics</subject><subject>PPAR alpha - metabolism</subject><subject>PPAR alpha - pharmacology</subject><subject>Proteins</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Receptors, Steroid - genetics</subject><subject>Receptors, Steroid - metabolism</subject><subject>Steroids</subject><subject>Thiolase</subject><subject>Transcription activation</subject><subject>Tumors</subject><issn>1347-9032</issn><issn>1349-7006</issn><issn>1349-7006</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqNks-O0zAQxiMEYpeFV0CREOLU4j-JHR8QWlXAIq3EAThbE2fSdZXaxXaW9sYj8Iw8Cc62lD8HVF880vy-0cynryhKSuY0v5erOeWVmklCxJwRouaEVoLMt_eK82Pj_l0tZ4pwdlY8inFFCBeVqh4WZ4xQzhjj50W6sjF5hyUYTLsBkvWuBNeVMWHwtisDGtwkH0rjwSR7C1ON203AGCe2G4N1y9IMvrdtgIQ_vn23rhsNZi2k8gY3WWIgGOv8Eh1GGx8XD3oYIj45_BfF57dvPi2uZtcf3r1fXF7PjKw4mfVAGt63UMmaMtMr1bZAGOUILQXVKtOpHpURTEL2QHQUKwIgqtqYvm0V4xfF6_3czdiusTPoUoBBb4JdQ9hpD1b_3XH2Ri_9rc4e1w2lTZ7w4jAh-C8jxqTXNhocBnDox6hl1ahKZvwEUjAma6ZOJqf9n_1DrvwYXLZMc8qobBSh5H8UawStZSNrkalmT5ngYwzYH22gZLqX6pWesqOn7OgpVPouVHqbpU__tPEo_JWiDDw_ABANDH0AZ2z8zTEluOCTR6_23Fc74O7kBfTi8uNU8Z_a1-tO</recordid><startdate>201004</startdate><enddate>201004</enddate><creator>Asano, Jumpei</creator><creator>Kudo, Toshihiro</creator><creator>Shimizu, Takeshi</creator><creator>Fan, Yang</creator><creator>Nanashima, Naoki</creator><creator>Yamana, Daisuke</creator><creator>Miura, Takuya</creator><creator>Yamada, Toshiyuki</creator><creator>Tsuchida, Shigeki</creator><general>Blackwell Publishing Ltd</general><general>Blackwell</general><general>John Wiley & Sons, Inc</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>8FE</scope><scope>8FH</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>GNUQQ</scope><scope>HCIFZ</scope><scope>LK8</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7TM</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>201004</creationdate><title>Histone acetylation and steroid receptor coactivator expression during clofibrate‐induced rat hepatocarcinogenesis</title><author>Asano, Jumpei ; Kudo, Toshihiro ; Shimizu, Takeshi ; Fan, Yang ; Nanashima, Naoki ; Yamana, Daisuke ; Miura, Takuya ; Yamada, Toshiyuki ; Tsuchida, Shigeki</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c7430-fa083fba47512cf99bba0213eab1a9b9cd9fe9c627a0096d1e40aa645ccfbb923</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Acetyl Coenzyme A - genetics</topic><topic>Acetyl Coenzyme A - metabolism</topic><topic>Acetyl Coenzyme A - pharmacology</topic><topic>Acetyl-CoA C-Acetyltransferase - genetics</topic><topic>Acetyl-CoA C-Acetyltransferase - metabolism</topic><topic>Acetylation</topic><topic>Animals</topic><topic>Antibodies</topic><topic>Biological and medical sciences</topic><topic>Carcinogens</topic><topic>Cell Transformation, Neoplastic - genetics</topic><topic>Cell Transformation, Neoplastic - metabolism</topic><topic>Clofibrate</topic><topic>Enzyme Induction</topic><topic>Enzymes</topic><topic>Epigenetics</topic><topic>Fatty acids</topic><topic>Fatty Acids - genetics</topic><topic>Fatty Acids - metabolism</topic><topic>Fatty Acids - pharmacology</topic><topic>Gastroenterology. Liver. Pancreas. Abdomen</topic><topic>Genes</topic><topic>Genotoxicity</topic><topic>Histone acetyltransferase</topic><topic>Histone H3</topic><topic>Histones - genetics</topic><topic>Histones - metabolism</topic><topic>Histones - pharmacology</topic><topic>Liver</topic><topic>Liver - drug effects</topic><topic>Liver - enzymology</topic><topic>Liver - metabolism</topic><topic>Liver Neoplasms, Experimental - chemically induced</topic><topic>Liver Neoplasms, Experimental - metabolism</topic><topic>Liver. Biliary tract. Portal circulation. Exocrine pancreas</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Nuclear Receptor Coactivator 3 - metabolism</topic><topic>Original</topic><topic>Oxidation</topic><topic>Peptides</topic><topic>Peroxisome proliferator-activated receptors</topic><topic>Peroxisome Proliferators - metabolism</topic><topic>Peroxisome Proliferators - pharmacology</topic><topic>Polymorphism, Genetic</topic><topic>PPAR alpha - genetics</topic><topic>PPAR alpha - metabolism</topic><topic>PPAR alpha - pharmacology</topic><topic>Proteins</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Receptors, Steroid - genetics</topic><topic>Receptors, Steroid - metabolism</topic><topic>Steroids</topic><topic>Thiolase</topic><topic>Transcription activation</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Asano, Jumpei</creatorcontrib><creatorcontrib>Kudo, Toshihiro</creatorcontrib><creatorcontrib>Shimizu, Takeshi</creatorcontrib><creatorcontrib>Fan, Yang</creatorcontrib><creatorcontrib>Nanashima, Naoki</creatorcontrib><creatorcontrib>Yamana, Daisuke</creatorcontrib><creatorcontrib>Miura, Takuya</creatorcontrib><creatorcontrib>Yamada, Toshiyuki</creatorcontrib><creatorcontrib>Tsuchida, Shigeki</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>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</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>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Biological Science Collection</collection><collection>Biological Science Database</collection><collection>Publicly Available Content Database</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>Nucleic Acids Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Cancer science</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext_linktorsrc</fulltext></delivery><addata><au>Asano, Jumpei</au><au>Kudo, Toshihiro</au><au>Shimizu, Takeshi</au><au>Fan, Yang</au><au>Nanashima, Naoki</au><au>Yamana, Daisuke</au><au>Miura, Takuya</au><au>Yamada, Toshiyuki</au><au>Tsuchida, Shigeki</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Histone acetylation and steroid receptor coactivator expression during clofibrate‐induced rat hepatocarcinogenesis</atitle><jtitle>Cancer science</jtitle><addtitle>Cancer Sci</addtitle><date>2010-04</date><risdate>2010</risdate><volume>101</volume><issue>4</issue><spage>869</spage><epage>875</epage><pages>869-875</pages><issn>1347-9032</issn><issn>1349-7006</issn><eissn>1349-7006</eissn><abstract>Peroxisome proliferators (PPs), non‐genotoxic rodent carcinogens, cause the induction of the peroxisomal fatty acid β‐oxidation system, including bifunctional enzyme (BE) and 3‐ketoacyl‐CoA thiolase (TH), in the liver. GST M1 gene is polymorphic in Sprague–Dawley rats, NC‐ and KS‐type. The KS‐type rats showed enhanced susceptibility to ethyl‐α‐chlorophenoxyisobutyrate (clofibrate, CF), one of the PPs. The degree of BE induction was higher in the KS‐type and preneoplastic foci developed after 6–8 weeks of treatment, whereas no foci developed in the NC‐type. In the preset study, factors involved in different BE inducibility were investigated. There were no differences in hepatic peroxisome proliferator‐activated receptor (PPAR) α levels between them. Among various coactivators for PPARα, only steroid receptor coactivator (SRC)‐3 level was higher in the KS‐type. To investigate the association between PPARα and SRC‐3 or other proteins, nuclear extracts from CF‐treated livers were applied to a PPARα column. In the KS‐type, 110, 72, and 42 kDa proteins were bound and these were identified as SRC‐3, BE, and TH, respectively. EMSA supported the binding of these proteins to PPARα associated to the BE enhancer in CF‐treated KS‐type, but not in the NC‐type. Histone H3 acetylation was increased 11‐fold in the KS‐type by CF treatment but not in the NC‐type. As BE and TH are responsible for acetyl‐CoA production and SRC‐3 possesses a histone acetyltransferase activity, these results suggest that enhanced BE induction in the KS‐type livers is due to acetylation‐mediated transcriptional activation and epigenetic mechanisms might be involved in CF‐induced rat hepatocarcinogenesis.
(Cancer Sci 2010; 101: 876–875)</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>20132223</pmid><doi>10.1111/j.1349-7006.2009.01460.x</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| identifier | ISSN: 1347-9032 |
| ispartof | Cancer science, 2010-04, Vol.101 (4), p.869-875 |
| issn | 1347-9032 1349-7006 1349-7006 |
| language | eng |
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| source | Wiley Online Library Open Access |
| subjects | Acetyl Coenzyme A - genetics Acetyl Coenzyme A - metabolism Acetyl Coenzyme A - pharmacology Acetyl-CoA C-Acetyltransferase - genetics Acetyl-CoA C-Acetyltransferase - metabolism Acetylation Animals Antibodies Biological and medical sciences Carcinogens Cell Transformation, Neoplastic - genetics Cell Transformation, Neoplastic - metabolism Clofibrate Enzyme Induction Enzymes Epigenetics Fatty acids Fatty Acids - genetics Fatty Acids - metabolism Fatty Acids - pharmacology Gastroenterology. Liver. Pancreas. Abdomen Genes Genotoxicity Histone acetyltransferase Histone H3 Histones - genetics Histones - metabolism Histones - pharmacology Liver Liver - drug effects Liver - enzymology Liver - metabolism Liver Neoplasms, Experimental - chemically induced Liver Neoplasms, Experimental - metabolism Liver. Biliary tract. Portal circulation. Exocrine pancreas Male Medical sciences Nuclear Receptor Coactivator 3 - metabolism Original Oxidation Peptides Peroxisome proliferator-activated receptors Peroxisome Proliferators - metabolism Peroxisome Proliferators - pharmacology Polymorphism, Genetic PPAR alpha - genetics PPAR alpha - metabolism PPAR alpha - pharmacology Proteins Rats Rats, Sprague-Dawley Receptors, Steroid - genetics Receptors, Steroid - metabolism Steroids Thiolase Transcription activation Tumors |
| title | Histone acetylation and steroid receptor coactivator expression during clofibrate‐induced rat hepatocarcinogenesis |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-17T03%3A56%3A47IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_24P&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Histone%20acetylation%20and%20steroid%20receptor%20coactivator%20expression%20during%20clofibrate%E2%80%90induced%20rat%20hepatocarcinogenesis&rft.jtitle=Cancer%20science&rft.au=Asano,%20Jumpei&rft.date=2010-04&rft.volume=101&rft.issue=4&rft.spage=869&rft.epage=875&rft.pages=869-875&rft.issn=1347-9032&rft.eissn=1349-7006&rft_id=info:doi/10.1111/j.1349-7006.2009.01460.x&rft_dat=%3Cproquest_24P%3E746227529%3C/proquest_24P%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2861578756&rft_id=info:pmid/20132223&rfr_iscdi=true |