Hepatitis B virus protein preS2 potentially promotes HCC development via its transcriptional activation of hTERT
Backgrounds and aims:Telomerase is significantly reactivated in hepatitis B virus (HBV)-associated hepatocellular carcinoma (HCC). Our previous studies showed that the transactivation unit of HBV surface (S) gene, preS2, could upregulate human telomerase reverse transcriptase (hTERT) expression and...
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| Veröffentlicht in: | Gut 2009-11, Vol.58 (11), p.1528-1537 |
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| creator | Luan, F Liu, H Gao, L Liu, J Sun, Z Ju, Y Hou, N Guo, C Liang, X Zhang, L Sun, W Ma, C |
| description | Backgrounds and aims:Telomerase is significantly reactivated in hepatitis B virus (HBV)-associated hepatocellular carcinoma (HCC). Our previous studies showed that the transactivation unit of HBV surface (S) gene, preS2, could upregulate human telomerase reverse transcriptase (hTERT) expression and telomerase activity of HepG2 cells. Here, we aim to explore the functions, and the underlying mechanisms, of this preS2-mediated hTERT upregulation during HCC development.Methods:An antisense blocking assay was performed on HBV-integrated HepG2.2.15 cells. The expression of hTERT was examined in clinical samples to test the role of the preS2-mediated hTERT upregulation in HCC development in vivo. In order to explore the mechanisms of preS2-mediated hTERT upregulation, co-transfection, reporter assays and electrophoretic mobility shift assays (EMSA) were performed.Results:Blocking preS2 expression reduced hTERT expression, telomerase activity, cell proliferation and tumorigenicity of HepG2.2.15. A region located between −349 and −329 bp upstream of the transcription initiation site of hTERT was identified as responsible for the preS2-mediated effect. preS2 interacted with the preS2-responsible region (PRR) and activated the hTERT promoter. Importantly, hTERT was also highly expressed in preS2-positive human HCC samples. All these findings strongly suggest that preS2 may promote HCC development via hTERT activation.Conclusions:HBV protein preS2 upregulates hTERT via the PRR element in promoting HCC development. |
| doi_str_mv | 10.1136/gut.2008.174029 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_734089074</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>734089074</sourcerecordid><originalsourceid>FETCH-LOGICAL-b427t-51e65a30f9d16e0e1bb46f7c47892ec24c732039332227047f1fba6b287a04883</originalsourceid><addsrcrecordid>eNqFkcuLFDEQxoMo7uzq2ZsERAShZyuPzuOo7eooi4I7eg3pnrRm7JdJetj9783QwwpePBUf36-KqvoQekZgTQgTlz_mtKYAak0kB6ofoBXhQhWMKvUQrQCILErJ9Rk6j3EPGVSaPEZnRIuSCAYrNG3cZJNPPuK3-ODDHPEUxuT8kKu7oXjKYkjedt3d0emzjHhTVXjnDq4bpz67udFinyJOwQ6xCX5Kfhxsh22T_MEeBR5b_HN79XX7BD1qbRfd01O9QN_eX22rTXH95cPH6s11UXMqU1ESJ0rLoNU7Ihw4UtdctLLhUmnqGsobySgwzRilVAKXLWlrK2qqpAWuFLtAr5a5eenfs4vJ9D42ruvs4MY5Gsk4KA2SZ_LFP-R-nENePxoipWacM0YydblQTRhjDK41U_C9DXeGgDlmYXIW5piFWbLIHc9Pc-e6d7u__On5GXh5AmxsbNfm5zU-3nOUAs03lpkrFs7H5G7vfRt-GSGZLM3n75WpQMLNJ_3OVJl_vfB1v__vln8AogGtRQ</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1779344331</pqid></control><display><type>article</type><title>Hepatitis B virus protein preS2 potentially promotes HCC development via its transcriptional activation of hTERT</title><source>MEDLINE</source><source>BMJ Journals - NESLi2</source><source>PubMed Central</source><creator>Luan, F ; Liu, H ; Gao, L ; Liu, J ; Sun, Z ; Ju, Y ; Hou, N ; Guo, C ; Liang, X ; Zhang, L ; Sun, W ; Ma, C</creator><creatorcontrib>Luan, F ; Liu, H ; Gao, L ; Liu, J ; Sun, Z ; Ju, Y ; Hou, N ; Guo, C ; Liang, X ; Zhang, L ; Sun, W ; Ma, C</creatorcontrib><description>Backgrounds and aims:Telomerase is significantly reactivated in hepatitis B virus (HBV)-associated hepatocellular carcinoma (HCC). Our previous studies showed that the transactivation unit of HBV surface (S) gene, preS2, could upregulate human telomerase reverse transcriptase (hTERT) expression and telomerase activity of HepG2 cells. Here, we aim to explore the functions, and the underlying mechanisms, of this preS2-mediated hTERT upregulation during HCC development.Methods:An antisense blocking assay was performed on HBV-integrated HepG2.2.15 cells. The expression of hTERT was examined in clinical samples to test the role of the preS2-mediated hTERT upregulation in HCC development in vivo. In order to explore the mechanisms of preS2-mediated hTERT upregulation, co-transfection, reporter assays and electrophoretic mobility shift assays (EMSA) were performed.Results:Blocking preS2 expression reduced hTERT expression, telomerase activity, cell proliferation and tumorigenicity of HepG2.2.15. A region located between −349 and −329 bp upstream of the transcription initiation site of hTERT was identified as responsible for the preS2-mediated effect. preS2 interacted with the preS2-responsible region (PRR) and activated the hTERT promoter. Importantly, hTERT was also highly expressed in preS2-positive human HCC samples. All these findings strongly suggest that preS2 may promote HCC development via hTERT activation.Conclusions:HBV protein preS2 upregulates hTERT via the PRR element in promoting HCC development.</description><identifier>ISSN: 0017-5749</identifier><identifier>EISSN: 1468-3288</identifier><identifier>DOI: 10.1136/gut.2008.174029</identifier><identifier>PMID: 19651630</identifier><identifier>CODEN: GUTTAK</identifier><language>eng</language><publisher>London: BMJ Publishing Group Ltd and British Society of Gastroenterology</publisher><subject>Adult ; Aged ; Amino acids ; Animals ; Antigens ; Biological and medical sciences ; Carcinoma, Hepatocellular - etiology ; Carcinoma, Hepatocellular - metabolism ; Carcinoma, Hepatocellular - pathology ; Carcinoma, Hepatocellular - virology ; Cell Line, Tumor ; Cell Proliferation ; Deoxyribonucleic acid ; DNA ; Enzyme Activation ; Female ; Gastroenterology. Liver. Pancreas. Abdomen ; Gene Expression Regulation, Neoplastic ; Hep G2 Cells ; Hepatitis ; Hepatitis B Surface Antigens - physiology ; Humans ; Laboratory animals ; Liver cancer ; Liver Neoplasms - etiology ; Liver Neoplasms - metabolism ; Liver Neoplasms - pathology ; Liver Neoplasms - virology ; Liver. Biliary tract. Portal circulation. Exocrine pancreas ; Male ; Medical sciences ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; Middle Aged ; Protein Precursors - antagonists & inhibitors ; Protein Precursors - physiology ; Proteins ; RNA, Antisense - metabolism ; Studies ; Telomerase ; Telomerase - genetics ; Telomerase - metabolism ; Transcription, Genetic ; Tumors ; Up-Regulation</subject><ispartof>Gut, 2009-11, Vol.58 (11), p.1528-1537</ispartof><rights>BMJ Publishing Group Ltd and British Society of Gastroenterology. All rights reserved.</rights><rights>2009 INIST-CNRS</rights><rights>Copyright: 2009 BMJ Publishing Group Ltd and British Society of Gastroenterology. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-b427t-51e65a30f9d16e0e1bb46f7c47892ec24c732039332227047f1fba6b287a04883</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttp://gut.bmj.com/content/58/11/1528.full.pdf$$EPDF$$P50$$Gbmj$$H</linktopdf><linktohtml>$$Uhttp://gut.bmj.com/content/58/11/1528.full$$EHTML$$P50$$Gbmj$$H</linktohtml><link.rule.ids>114,115,314,776,780,3182,23551,27903,27904,77346,77377</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=22023205$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19651630$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Luan, F</creatorcontrib><creatorcontrib>Liu, H</creatorcontrib><creatorcontrib>Gao, L</creatorcontrib><creatorcontrib>Liu, J</creatorcontrib><creatorcontrib>Sun, Z</creatorcontrib><creatorcontrib>Ju, Y</creatorcontrib><creatorcontrib>Hou, N</creatorcontrib><creatorcontrib>Guo, C</creatorcontrib><creatorcontrib>Liang, X</creatorcontrib><creatorcontrib>Zhang, L</creatorcontrib><creatorcontrib>Sun, W</creatorcontrib><creatorcontrib>Ma, C</creatorcontrib><title>Hepatitis B virus protein preS2 potentially promotes HCC development via its transcriptional activation of hTERT</title><title>Gut</title><addtitle>Gut</addtitle><description>Backgrounds and aims:Telomerase is significantly reactivated in hepatitis B virus (HBV)-associated hepatocellular carcinoma (HCC). Our previous studies showed that the transactivation unit of HBV surface (S) gene, preS2, could upregulate human telomerase reverse transcriptase (hTERT) expression and telomerase activity of HepG2 cells. Here, we aim to explore the functions, and the underlying mechanisms, of this preS2-mediated hTERT upregulation during HCC development.Methods:An antisense blocking assay was performed on HBV-integrated HepG2.2.15 cells. The expression of hTERT was examined in clinical samples to test the role of the preS2-mediated hTERT upregulation in HCC development in vivo. In order to explore the mechanisms of preS2-mediated hTERT upregulation, co-transfection, reporter assays and electrophoretic mobility shift assays (EMSA) were performed.Results:Blocking preS2 expression reduced hTERT expression, telomerase activity, cell proliferation and tumorigenicity of HepG2.2.15. A region located between −349 and −329 bp upstream of the transcription initiation site of hTERT was identified as responsible for the preS2-mediated effect. preS2 interacted with the preS2-responsible region (PRR) and activated the hTERT promoter. Importantly, hTERT was also highly expressed in preS2-positive human HCC samples. All these findings strongly suggest that preS2 may promote HCC development via hTERT activation.Conclusions:HBV protein preS2 upregulates hTERT via the PRR element in promoting HCC development.</description><subject>Adult</subject><subject>Aged</subject><subject>Amino acids</subject><subject>Animals</subject><subject>Antigens</subject><subject>Biological and medical sciences</subject><subject>Carcinoma, Hepatocellular - etiology</subject><subject>Carcinoma, Hepatocellular - metabolism</subject><subject>Carcinoma, Hepatocellular - pathology</subject><subject>Carcinoma, Hepatocellular - virology</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation</subject><subject>Deoxyribonucleic acid</subject><subject>DNA</subject><subject>Enzyme Activation</subject><subject>Female</subject><subject>Gastroenterology. Liver. Pancreas. Abdomen</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Hep G2 Cells</subject><subject>Hepatitis</subject><subject>Hepatitis B Surface Antigens - physiology</subject><subject>Humans</subject><subject>Laboratory animals</subject><subject>Liver cancer</subject><subject>Liver Neoplasms - etiology</subject><subject>Liver Neoplasms - metabolism</subject><subject>Liver Neoplasms - pathology</subject><subject>Liver Neoplasms - virology</subject><subject>Liver. Biliary tract. Portal circulation. Exocrine pancreas</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Mice, Nude</subject><subject>Middle Aged</subject><subject>Protein Precursors - antagonists & inhibitors</subject><subject>Protein Precursors - physiology</subject><subject>Proteins</subject><subject>RNA, Antisense - metabolism</subject><subject>Studies</subject><subject>Telomerase</subject><subject>Telomerase - genetics</subject><subject>Telomerase - metabolism</subject><subject>Transcription, Genetic</subject><subject>Tumors</subject><subject>Up-Regulation</subject><issn>0017-5749</issn><issn>1468-3288</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNqFkcuLFDEQxoMo7uzq2ZsERAShZyuPzuOo7eooi4I7eg3pnrRm7JdJetj9783QwwpePBUf36-KqvoQekZgTQgTlz_mtKYAak0kB6ofoBXhQhWMKvUQrQCILErJ9Rk6j3EPGVSaPEZnRIuSCAYrNG3cZJNPPuK3-ODDHPEUxuT8kKu7oXjKYkjedt3d0emzjHhTVXjnDq4bpz67udFinyJOwQ6xCX5Kfhxsh22T_MEeBR5b_HN79XX7BD1qbRfd01O9QN_eX22rTXH95cPH6s11UXMqU1ESJ0rLoNU7Ihw4UtdctLLhUmnqGsobySgwzRilVAKXLWlrK2qqpAWuFLtAr5a5eenfs4vJ9D42ruvs4MY5Gsk4KA2SZ_LFP-R-nENePxoipWacM0YydblQTRhjDK41U_C9DXeGgDlmYXIW5piFWbLIHc9Pc-e6d7u__On5GXh5AmxsbNfm5zU-3nOUAs03lpkrFs7H5G7vfRt-GSGZLM3n75WpQMLNJ_3OVJl_vfB1v__vln8AogGtRQ</recordid><startdate>20091101</startdate><enddate>20091101</enddate><creator>Luan, F</creator><creator>Liu, H</creator><creator>Gao, L</creator><creator>Liu, J</creator><creator>Sun, Z</creator><creator>Ju, Y</creator><creator>Hou, N</creator><creator>Guo, C</creator><creator>Liang, X</creator><creator>Zhang, L</creator><creator>Sun, W</creator><creator>Ma, C</creator><general>BMJ Publishing Group Ltd and British Society of Gastroenterology</general><general>BMJ Publishing Group</general><general>BMJ Publishing Group LTD</general><scope>BSCLL</scope><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>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88I</scope><scope>8AF</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>BTHHO</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>7X8</scope></search><sort><creationdate>20091101</creationdate><title>Hepatitis B virus protein preS2 potentially promotes HCC development via its transcriptional activation of hTERT</title><author>Luan, F ; Liu, H ; Gao, L ; Liu, J ; Sun, Z ; Ju, Y ; Hou, N ; Guo, C ; Liang, X ; Zhang, L ; Sun, W ; Ma, C</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-b427t-51e65a30f9d16e0e1bb46f7c47892ec24c732039332227047f1fba6b287a04883</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Amino acids</topic><topic>Animals</topic><topic>Antigens</topic><topic>Biological and medical sciences</topic><topic>Carcinoma, Hepatocellular - etiology</topic><topic>Carcinoma, Hepatocellular - metabolism</topic><topic>Carcinoma, Hepatocellular - pathology</topic><topic>Carcinoma, Hepatocellular - virology</topic><topic>Cell Line, Tumor</topic><topic>Cell Proliferation</topic><topic>Deoxyribonucleic acid</topic><topic>DNA</topic><topic>Enzyme Activation</topic><topic>Female</topic><topic>Gastroenterology. Liver. Pancreas. Abdomen</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Hep G2 Cells</topic><topic>Hepatitis</topic><topic>Hepatitis B Surface Antigens - physiology</topic><topic>Humans</topic><topic>Laboratory animals</topic><topic>Liver cancer</topic><topic>Liver Neoplasms - etiology</topic><topic>Liver Neoplasms - metabolism</topic><topic>Liver Neoplasms - pathology</topic><topic>Liver Neoplasms - virology</topic><topic>Liver. Biliary tract. Portal circulation. Exocrine pancreas</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Mice, Nude</topic><topic>Middle Aged</topic><topic>Protein Precursors - antagonists & inhibitors</topic><topic>Protein Precursors - physiology</topic><topic>Proteins</topic><topic>RNA, Antisense - metabolism</topic><topic>Studies</topic><topic>Telomerase</topic><topic>Telomerase - genetics</topic><topic>Telomerase - metabolism</topic><topic>Transcription, Genetic</topic><topic>Tumors</topic><topic>Up-Regulation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Luan, F</creatorcontrib><creatorcontrib>Liu, H</creatorcontrib><creatorcontrib>Gao, L</creatorcontrib><creatorcontrib>Liu, J</creatorcontrib><creatorcontrib>Sun, Z</creatorcontrib><creatorcontrib>Ju, Y</creatorcontrib><creatorcontrib>Hou, N</creatorcontrib><creatorcontrib>Guo, C</creatorcontrib><creatorcontrib>Liang, X</creatorcontrib><creatorcontrib>Zhang, L</creatorcontrib><creatorcontrib>Sun, W</creatorcontrib><creatorcontrib>Ma, C</creatorcontrib><collection>Istex</collection><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>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>STEM 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>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>BMJ Journals</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</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>Science Database</collection><collection>Biological Science 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 Basic</collection><collection>MEDLINE - Academic</collection><jtitle>Gut</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Luan, F</au><au>Liu, H</au><au>Gao, L</au><au>Liu, J</au><au>Sun, Z</au><au>Ju, Y</au><au>Hou, N</au><au>Guo, C</au><au>Liang, X</au><au>Zhang, L</au><au>Sun, W</au><au>Ma, C</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Hepatitis B virus protein preS2 potentially promotes HCC development via its transcriptional activation of hTERT</atitle><jtitle>Gut</jtitle><addtitle>Gut</addtitle><date>2009-11-01</date><risdate>2009</risdate><volume>58</volume><issue>11</issue><spage>1528</spage><epage>1537</epage><pages>1528-1537</pages><issn>0017-5749</issn><eissn>1468-3288</eissn><coden>GUTTAK</coden><abstract>Backgrounds and aims:Telomerase is significantly reactivated in hepatitis B virus (HBV)-associated hepatocellular carcinoma (HCC). Our previous studies showed that the transactivation unit of HBV surface (S) gene, preS2, could upregulate human telomerase reverse transcriptase (hTERT) expression and telomerase activity of HepG2 cells. Here, we aim to explore the functions, and the underlying mechanisms, of this preS2-mediated hTERT upregulation during HCC development.Methods:An antisense blocking assay was performed on HBV-integrated HepG2.2.15 cells. The expression of hTERT was examined in clinical samples to test the role of the preS2-mediated hTERT upregulation in HCC development in vivo. In order to explore the mechanisms of preS2-mediated hTERT upregulation, co-transfection, reporter assays and electrophoretic mobility shift assays (EMSA) were performed.Results:Blocking preS2 expression reduced hTERT expression, telomerase activity, cell proliferation and tumorigenicity of HepG2.2.15. A region located between −349 and −329 bp upstream of the transcription initiation site of hTERT was identified as responsible for the preS2-mediated effect. preS2 interacted with the preS2-responsible region (PRR) and activated the hTERT promoter. Importantly, hTERT was also highly expressed in preS2-positive human HCC samples. All these findings strongly suggest that preS2 may promote HCC development via hTERT activation.Conclusions:HBV protein preS2 upregulates hTERT via the PRR element in promoting HCC development.</abstract><cop>London</cop><pub>BMJ Publishing Group Ltd and British Society of Gastroenterology</pub><pmid>19651630</pmid><doi>10.1136/gut.2008.174029</doi><tpages>10</tpages></addata></record> |
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| subjects | Adult Aged Amino acids Animals Antigens Biological and medical sciences Carcinoma, Hepatocellular - etiology Carcinoma, Hepatocellular - metabolism Carcinoma, Hepatocellular - pathology Carcinoma, Hepatocellular - virology Cell Line, Tumor Cell Proliferation Deoxyribonucleic acid DNA Enzyme Activation Female Gastroenterology. Liver. Pancreas. Abdomen Gene Expression Regulation, Neoplastic Hep G2 Cells Hepatitis Hepatitis B Surface Antigens - physiology Humans Laboratory animals Liver cancer Liver Neoplasms - etiology Liver Neoplasms - metabolism Liver Neoplasms - pathology Liver Neoplasms - virology Liver. Biliary tract. Portal circulation. Exocrine pancreas Male Medical sciences Mice Mice, Inbred BALB C Mice, Nude Middle Aged Protein Precursors - antagonists & inhibitors Protein Precursors - physiology Proteins RNA, Antisense - metabolism Studies Telomerase Telomerase - genetics Telomerase - metabolism Transcription, Genetic Tumors Up-Regulation |
| title | Hepatitis B virus protein preS2 potentially promotes HCC development via its transcriptional activation of hTERT |
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