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Overexpression of myocyte enhancer factor 2 and histone hyperacetylation in hepatocellular carcinoma
Purpose It has been indicated that activated hepatic stellate cells (HSCs) play key roles on the pathogenesis of hepatocellular carcinoma (HCC). The purpose of the study was to investigate the potential mechanism in it. Methods Activation of HSCs, the expression of myocyte enhancer factor 2 (MEF2),...
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| Published in: | Journal of cancer research and clinical oncology 2008-01, Vol.134 (1), p.83-91 |
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| container_title | Journal of cancer research and clinical oncology |
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| creator | Bai, XueLi Wu, LiHua Liang, TingBo Liu, ZhiQiang Li, JunJian Li, DongLin Xie, HaiYang Yin, ShengYong Yu, Jun Lin, Qi Zheng, ShuSen |
| description | Purpose
It has been indicated that activated hepatic stellate cells (HSCs) play key roles on the pathogenesis of hepatocellular carcinoma (HCC). The purpose of the study was to investigate the potential mechanism in it.
Methods
Activation of HSCs, the expression of myocyte enhancer factor 2 (MEF2), class II histone deacetylases (II HDACs) and histone acetylation were analyzed in specimens of primary HCCs, cirrhotic and normal livers. Activated HSCs were identified using anti-a-smooth muscle actin (a-SMA) by Immunohistochemistry (IHC). The levels of expression of MEF2A, MEF2C and II HDACs mRNA and protein were measured by real time quantitative PCR and western blot (WB). Histone acetylation was assessed using anti-acetyl-histone H3, -H4 by WB and IHC. A
P
value |
| doi_str_mv | 10.1007/s00432-007-0252-7 |
| format | article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_journals_220509695</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1380115571</sourcerecordid><originalsourceid>FETCH-LOGICAL-c434t-276c21e68a347c855f2ad4368de9ca7abde12d03bb2c76e1b6f1acc8872a4d683</originalsourceid><addsrcrecordid>eNp1kE1LxDAQhoMo7rr6A7xIEDxW89Em7VHEL1jYi57LNJ26XbpJTbpi_70pu7AnT5lMnncmPIRcc3bPGdMPgbFUiiSWCROZSPQJmfOpw6XMTsmccc2TTHA1IxchbFi8Z1qckxnXinOt8zmpVz_o8bf3GELrLHUN3Y7OjANStGuwBj1twAzOU0HB1nTdhsFZpOuxRw8Gh7GDYUq2lq6xh8EZ7LpdB54a8Ka1bguX5KyBLuDV4VyQz5fnj6e3ZLl6fX96XCYmlemQCK2M4KhykKk2eZY1AupUqrzGwoCGqkYuaiarShitkFeq4WBMnmsBaa1yuSC3-7m9d987DEO5cTtv48pSCJaxQhVZhPgeMt6F4LEpe99uwY8lZ-WktdxrLady0lrqmLk5DN5VW6yPiYPHCNwdAAgGusZHc204ckWRaibTyIk9F-KT_UJ__OH_2_8A4JeRRA</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>220509695</pqid></control><display><type>article</type><title>Overexpression of myocyte enhancer factor 2 and histone hyperacetylation in hepatocellular carcinoma</title><source>Springer Nature</source><creator>Bai, XueLi ; Wu, LiHua ; Liang, TingBo ; Liu, ZhiQiang ; Li, JunJian ; Li, DongLin ; Xie, HaiYang ; Yin, ShengYong ; Yu, Jun ; Lin, Qi ; Zheng, ShuSen</creator><creatorcontrib>Bai, XueLi ; Wu, LiHua ; Liang, TingBo ; Liu, ZhiQiang ; Li, JunJian ; Li, DongLin ; Xie, HaiYang ; Yin, ShengYong ; Yu, Jun ; Lin, Qi ; Zheng, ShuSen</creatorcontrib><description>Purpose
It has been indicated that activated hepatic stellate cells (HSCs) play key roles on the pathogenesis of hepatocellular carcinoma (HCC). The purpose of the study was to investigate the potential mechanism in it.
Methods
Activation of HSCs, the expression of myocyte enhancer factor 2 (MEF2), class II histone deacetylases (II HDACs) and histone acetylation were analyzed in specimens of primary HCCs, cirrhotic and normal livers. Activated HSCs were identified using anti-a-smooth muscle actin (a-SMA) by Immunohistochemistry (IHC). The levels of expression of MEF2A, MEF2C and II HDACs mRNA and protein were measured by real time quantitative PCR and western blot (WB). Histone acetylation was assessed using anti-acetyl-histone H3, -H4 by WB and IHC. A
P
value < 0.05 was considered statistically significant.
Results
A-SMA positive activated HSCs were more prominent in HCCs and cirrhotic livers than in normal livers, accompanied by marked expression of MEF2A and MEF2C. The expression of MEF2A, MEF2C and II HDACs, both mRNA and protein, were much more enhanced in HCCs than those in cirrhotic and normal livers (
P
< 0.05). Histone H3 and H4 were hyperacetylated in HCCs compared with those in cirrhotic and normal livers (
P
< 0.05). The correlation coefficients between the expression of MEF2 and II HDACs, acetyl-histones were all beyond 0.5.
Conclusions
These data showed a potential molecular mechanism that activated HSCs participate in the pathogenesis of HCCs by overexpression of MEF2 and its consequent impact on histone hyperacetylation. Further investigations aimed at interfering MEF2 expression are needed.</description><identifier>ISSN: 0171-5216</identifier><identifier>EISSN: 1432-1335</identifier><identifier>DOI: 10.1007/s00432-007-0252-7</identifier><identifier>PMID: 17611778</identifier><identifier>CODEN: JCROD7</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer-Verlag</publisher><subject>Acetylation - drug effects ; Antineoplastic agents ; Biological and medical sciences ; Blotting, Western ; Cancer ; Cancer Research ; Carcinoma, Hepatocellular - metabolism ; Carcinoma, Hepatocellular - pathology ; Carcinoma, Hepatocellular - therapy ; Gastroenterology. Liver. Pancreas. Abdomen ; Gene expression ; Hematology ; Histone Deacetylases - genetics ; Histone Deacetylases - metabolism ; Histones - metabolism ; Humans ; Immunoenzyme Techniques ; Internal Medicine ; Liver - cytology ; Liver - metabolism ; Liver Cirrhosis - metabolism ; Liver Cirrhosis - pathology ; Liver Cirrhosis - therapy ; Liver diseases ; Liver Neoplasms - metabolism ; Liver Neoplasms - pathology ; Liver. Biliary tract. Portal circulation. Exocrine pancreas ; MADS Domain Proteins - genetics ; MADS Domain Proteins - metabolism ; Medical sciences ; Medicine ; Medicine & Public Health ; MEF2 Transcription Factors ; Myogenic Regulatory Factors - genetics ; Myogenic Regulatory Factors - metabolism ; Oncology ; Original Paper ; Pathology ; Pharmacology. Drug treatments ; Proteins ; Reverse Transcriptase Polymerase Chain Reaction ; RNA, Messenger - genetics ; RNA, Messenger - metabolism ; Tissue Array Analysis ; Tumors</subject><ispartof>Journal of cancer research and clinical oncology, 2008-01, Vol.134 (1), p.83-91</ispartof><rights>Springer-Verlag 2007</rights><rights>2008 INIST-CNRS</rights><rights>Springer-Verlag 2008</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c434t-276c21e68a347c855f2ad4368de9ca7abde12d03bb2c76e1b6f1acc8872a4d683</citedby><cites>FETCH-LOGICAL-c434t-276c21e68a347c855f2ad4368de9ca7abde12d03bb2c76e1b6f1acc8872a4d683</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=19947034$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17611778$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Bai, XueLi</creatorcontrib><creatorcontrib>Wu, LiHua</creatorcontrib><creatorcontrib>Liang, TingBo</creatorcontrib><creatorcontrib>Liu, ZhiQiang</creatorcontrib><creatorcontrib>Li, JunJian</creatorcontrib><creatorcontrib>Li, DongLin</creatorcontrib><creatorcontrib>Xie, HaiYang</creatorcontrib><creatorcontrib>Yin, ShengYong</creatorcontrib><creatorcontrib>Yu, Jun</creatorcontrib><creatorcontrib>Lin, Qi</creatorcontrib><creatorcontrib>Zheng, ShuSen</creatorcontrib><title>Overexpression of myocyte enhancer factor 2 and histone hyperacetylation in hepatocellular carcinoma</title><title>Journal of cancer research and clinical oncology</title><addtitle>J Cancer Res Clin Oncol</addtitle><addtitle>J Cancer Res Clin Oncol</addtitle><description>Purpose
It has been indicated that activated hepatic stellate cells (HSCs) play key roles on the pathogenesis of hepatocellular carcinoma (HCC). The purpose of the study was to investigate the potential mechanism in it.
Methods
Activation of HSCs, the expression of myocyte enhancer factor 2 (MEF2), class II histone deacetylases (II HDACs) and histone acetylation were analyzed in specimens of primary HCCs, cirrhotic and normal livers. Activated HSCs were identified using anti-a-smooth muscle actin (a-SMA) by Immunohistochemistry (IHC). The levels of expression of MEF2A, MEF2C and II HDACs mRNA and protein were measured by real time quantitative PCR and western blot (WB). Histone acetylation was assessed using anti-acetyl-histone H3, -H4 by WB and IHC. A
P
value < 0.05 was considered statistically significant.
Results
A-SMA positive activated HSCs were more prominent in HCCs and cirrhotic livers than in normal livers, accompanied by marked expression of MEF2A and MEF2C. The expression of MEF2A, MEF2C and II HDACs, both mRNA and protein, were much more enhanced in HCCs than those in cirrhotic and normal livers (
P
< 0.05). Histone H3 and H4 were hyperacetylated in HCCs compared with those in cirrhotic and normal livers (
P
< 0.05). The correlation coefficients between the expression of MEF2 and II HDACs, acetyl-histones were all beyond 0.5.
Conclusions
These data showed a potential molecular mechanism that activated HSCs participate in the pathogenesis of HCCs by overexpression of MEF2 and its consequent impact on histone hyperacetylation. Further investigations aimed at interfering MEF2 expression are needed.</description><subject>Acetylation - drug effects</subject><subject>Antineoplastic agents</subject><subject>Biological and medical sciences</subject><subject>Blotting, Western</subject><subject>Cancer</subject><subject>Cancer Research</subject><subject>Carcinoma, Hepatocellular - metabolism</subject><subject>Carcinoma, Hepatocellular - pathology</subject><subject>Carcinoma, Hepatocellular - therapy</subject><subject>Gastroenterology. Liver. Pancreas. Abdomen</subject><subject>Gene expression</subject><subject>Hematology</subject><subject>Histone Deacetylases - genetics</subject><subject>Histone Deacetylases - metabolism</subject><subject>Histones - metabolism</subject><subject>Humans</subject><subject>Immunoenzyme Techniques</subject><subject>Internal Medicine</subject><subject>Liver - cytology</subject><subject>Liver - metabolism</subject><subject>Liver Cirrhosis - metabolism</subject><subject>Liver Cirrhosis - pathology</subject><subject>Liver Cirrhosis - therapy</subject><subject>Liver diseases</subject><subject>Liver Neoplasms - metabolism</subject><subject>Liver Neoplasms - pathology</subject><subject>Liver. Biliary tract. Portal circulation. Exocrine pancreas</subject><subject>MADS Domain Proteins - genetics</subject><subject>MADS Domain Proteins - metabolism</subject><subject>Medical sciences</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>MEF2 Transcription Factors</subject><subject>Myogenic Regulatory Factors - genetics</subject><subject>Myogenic Regulatory Factors - metabolism</subject><subject>Oncology</subject><subject>Original Paper</subject><subject>Pathology</subject><subject>Pharmacology. Drug treatments</subject><subject>Proteins</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>RNA, Messenger - genetics</subject><subject>RNA, Messenger - metabolism</subject><subject>Tissue Array Analysis</subject><subject>Tumors</subject><issn>0171-5216</issn><issn>1432-1335</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><recordid>eNp1kE1LxDAQhoMo7rr6A7xIEDxW89Em7VHEL1jYi57LNJ26XbpJTbpi_70pu7AnT5lMnncmPIRcc3bPGdMPgbFUiiSWCROZSPQJmfOpw6XMTsmccc2TTHA1IxchbFi8Z1qckxnXinOt8zmpVz_o8bf3GELrLHUN3Y7OjANStGuwBj1twAzOU0HB1nTdhsFZpOuxRw8Gh7GDYUq2lq6xh8EZ7LpdB54a8Ka1bguX5KyBLuDV4VyQz5fnj6e3ZLl6fX96XCYmlemQCK2M4KhykKk2eZY1AupUqrzGwoCGqkYuaiarShitkFeq4WBMnmsBaa1yuSC3-7m9d987DEO5cTtv48pSCJaxQhVZhPgeMt6F4LEpe99uwY8lZ-WktdxrLady0lrqmLk5DN5VW6yPiYPHCNwdAAgGusZHc204ckWRaibTyIk9F-KT_UJ__OH_2_8A4JeRRA</recordid><startdate>20080101</startdate><enddate>20080101</enddate><creator>Bai, XueLi</creator><creator>Wu, LiHua</creator><creator>Liang, TingBo</creator><creator>Liu, ZhiQiang</creator><creator>Li, JunJian</creator><creator>Li, DongLin</creator><creator>Xie, HaiYang</creator><creator>Yin, ShengYong</creator><creator>Yu, Jun</creator><creator>Lin, Qi</creator><creator>Zheng, ShuSen</creator><general>Springer-Verlag</general><general>Springer</general><general>Springer Nature B.V</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>3V.</scope><scope>7TO</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope></search><sort><creationdate>20080101</creationdate><title>Overexpression of myocyte enhancer factor 2 and histone hyperacetylation in hepatocellular carcinoma</title><author>Bai, XueLi ; Wu, LiHua ; Liang, TingBo ; Liu, ZhiQiang ; Li, JunJian ; Li, DongLin ; Xie, HaiYang ; Yin, ShengYong ; Yu, Jun ; Lin, Qi ; Zheng, ShuSen</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c434t-276c21e68a347c855f2ad4368de9ca7abde12d03bb2c76e1b6f1acc8872a4d683</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Acetylation - drug effects</topic><topic>Antineoplastic agents</topic><topic>Biological and medical sciences</topic><topic>Blotting, Western</topic><topic>Cancer</topic><topic>Cancer Research</topic><topic>Carcinoma, Hepatocellular - metabolism</topic><topic>Carcinoma, Hepatocellular - pathology</topic><topic>Carcinoma, Hepatocellular - therapy</topic><topic>Gastroenterology. Liver. Pancreas. Abdomen</topic><topic>Gene expression</topic><topic>Hematology</topic><topic>Histone Deacetylases - genetics</topic><topic>Histone Deacetylases - metabolism</topic><topic>Histones - metabolism</topic><topic>Humans</topic><topic>Immunoenzyme Techniques</topic><topic>Internal Medicine</topic><topic>Liver - cytology</topic><topic>Liver - metabolism</topic><topic>Liver Cirrhosis - metabolism</topic><topic>Liver Cirrhosis - pathology</topic><topic>Liver Cirrhosis - therapy</topic><topic>Liver diseases</topic><topic>Liver Neoplasms - metabolism</topic><topic>Liver Neoplasms - pathology</topic><topic>Liver. Biliary tract. Portal circulation. Exocrine pancreas</topic><topic>MADS Domain Proteins - genetics</topic><topic>MADS Domain Proteins - metabolism</topic><topic>Medical sciences</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>MEF2 Transcription Factors</topic><topic>Myogenic Regulatory Factors - genetics</topic><topic>Myogenic Regulatory Factors - metabolism</topic><topic>Oncology</topic><topic>Original Paper</topic><topic>Pathology</topic><topic>Pharmacology. Drug treatments</topic><topic>Proteins</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>RNA, Messenger - genetics</topic><topic>RNA, Messenger - metabolism</topic><topic>Tissue Array Analysis</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Bai, XueLi</creatorcontrib><creatorcontrib>Wu, LiHua</creatorcontrib><creatorcontrib>Liang, TingBo</creatorcontrib><creatorcontrib>Liu, ZhiQiang</creatorcontrib><creatorcontrib>Li, JunJian</creatorcontrib><creatorcontrib>Li, DongLin</creatorcontrib><creatorcontrib>Xie, HaiYang</creatorcontrib><creatorcontrib>Yin, ShengYong</creatorcontrib><creatorcontrib>Yu, Jun</creatorcontrib><creatorcontrib>Lin, Qi</creatorcontrib><creatorcontrib>Zheng, ShuSen</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 Central (Corporate)</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</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)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</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>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest research library</collection><collection>Research Library (Corporate)</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><jtitle>Journal of cancer research and clinical oncology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Bai, XueLi</au><au>Wu, LiHua</au><au>Liang, TingBo</au><au>Liu, ZhiQiang</au><au>Li, JunJian</au><au>Li, DongLin</au><au>Xie, HaiYang</au><au>Yin, ShengYong</au><au>Yu, Jun</au><au>Lin, Qi</au><au>Zheng, ShuSen</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Overexpression of myocyte enhancer factor 2 and histone hyperacetylation in hepatocellular carcinoma</atitle><jtitle>Journal of cancer research and clinical oncology</jtitle><stitle>J Cancer Res Clin Oncol</stitle><addtitle>J Cancer Res Clin Oncol</addtitle><date>2008-01-01</date><risdate>2008</risdate><volume>134</volume><issue>1</issue><spage>83</spage><epage>91</epage><pages>83-91</pages><issn>0171-5216</issn><eissn>1432-1335</eissn><coden>JCROD7</coden><abstract>Purpose
It has been indicated that activated hepatic stellate cells (HSCs) play key roles on the pathogenesis of hepatocellular carcinoma (HCC). The purpose of the study was to investigate the potential mechanism in it.
Methods
Activation of HSCs, the expression of myocyte enhancer factor 2 (MEF2), class II histone deacetylases (II HDACs) and histone acetylation were analyzed in specimens of primary HCCs, cirrhotic and normal livers. Activated HSCs were identified using anti-a-smooth muscle actin (a-SMA) by Immunohistochemistry (IHC). The levels of expression of MEF2A, MEF2C and II HDACs mRNA and protein were measured by real time quantitative PCR and western blot (WB). Histone acetylation was assessed using anti-acetyl-histone H3, -H4 by WB and IHC. A
P
value < 0.05 was considered statistically significant.
Results
A-SMA positive activated HSCs were more prominent in HCCs and cirrhotic livers than in normal livers, accompanied by marked expression of MEF2A and MEF2C. The expression of MEF2A, MEF2C and II HDACs, both mRNA and protein, were much more enhanced in HCCs than those in cirrhotic and normal livers (
P
< 0.05). Histone H3 and H4 were hyperacetylated in HCCs compared with those in cirrhotic and normal livers (
P
< 0.05). The correlation coefficients between the expression of MEF2 and II HDACs, acetyl-histones were all beyond 0.5.
Conclusions
These data showed a potential molecular mechanism that activated HSCs participate in the pathogenesis of HCCs by overexpression of MEF2 and its consequent impact on histone hyperacetylation. Further investigations aimed at interfering MEF2 expression are needed.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer-Verlag</pub><pmid>17611778</pmid><doi>10.1007/s00432-007-0252-7</doi><tpages>9</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0171-5216 |
| ispartof | Journal of cancer research and clinical oncology, 2008-01, Vol.134 (1), p.83-91 |
| issn | 0171-5216 1432-1335 |
| language | eng |
| recordid | cdi_proquest_journals_220509695 |
| source | Springer Nature |
| subjects | Acetylation - drug effects Antineoplastic agents Biological and medical sciences Blotting, Western Cancer Cancer Research Carcinoma, Hepatocellular - metabolism Carcinoma, Hepatocellular - pathology Carcinoma, Hepatocellular - therapy Gastroenterology. Liver. Pancreas. Abdomen Gene expression Hematology Histone Deacetylases - genetics Histone Deacetylases - metabolism Histones - metabolism Humans Immunoenzyme Techniques Internal Medicine Liver - cytology Liver - metabolism Liver Cirrhosis - metabolism Liver Cirrhosis - pathology Liver Cirrhosis - therapy Liver diseases Liver Neoplasms - metabolism Liver Neoplasms - pathology Liver. Biliary tract. Portal circulation. Exocrine pancreas MADS Domain Proteins - genetics MADS Domain Proteins - metabolism Medical sciences Medicine Medicine & Public Health MEF2 Transcription Factors Myogenic Regulatory Factors - genetics Myogenic Regulatory Factors - metabolism Oncology Original Paper Pathology Pharmacology. Drug treatments Proteins Reverse Transcriptase Polymerase Chain Reaction RNA, Messenger - genetics RNA, Messenger - metabolism Tissue Array Analysis Tumors |
| title | Overexpression of myocyte enhancer factor 2 and histone hyperacetylation in hepatocellular carcinoma |
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