The N-terminal common domain of simian virus 40 large T and small t antigens acts as a transformation suppressor of the HER-2/neu oncogene
Overexpression of HER-2/neu (also known as c-erbB-2) proto-oncogene frequently occurs in many different types of human cancers, including ovarian carcinoma, and is known to enhance tumor metastasis and chemoresistance. Previous studies showed that inhibition of HER-2/neu expression by various agents...
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| Veröffentlicht in: | Oncogene 2000-05, Vol.19 (22), p.2704-2713 |
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| description | Overexpression of HER-2/neu (also known as c-erbB-2) proto-oncogene frequently occurs in many different types of human cancers, including ovarian carcinoma, and is known to enhance tumor metastasis and chemoresistance. Previous studies showed that inhibition of HER-2/neu expression by various agents, such as adenovirus E1A and simian virus 40 large T, can lead to suppression of tumorigenicity of HER-2/neu-overexpressing cancer cells. Here we report that T/t-common, which contains the N-terminal common domain of simian virus 40 large T and small t antigens, could specifically repress the HER-2/neu promoter. When the coding sequence of T/t-common was stably transfected into the HER-2/neu-overexpressing human ovarian carcinoma SK-OV-3 cells, the expression of HER-2/neu was dramatically reduced by the expression of T/t-common. Accordingly the tumorigenic potential of these T/t-common-expressing clones, including the ability to grow anchorage-independently and the ability to induce tumor in nu/nu mice, was also drastically suppressed. Furthermore, when T/t-common was transiently cotransfected with the activated genomic neu into NIH3T3 cells, the transforming activity of the latter was suppressed by T/t-common in soft-agarose microcolony formation assays. Taken together, these data suggest that T/t-common may act as a transformation suppressor of the HER-2/neu oncogene. Oncogene (2000). |
| doi_str_mv | 10.1038/sj.onc.1203582 |
| format | Article |
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Previous studies showed that inhibition of HER-2/neu expression by various agents, such as adenovirus E1A and simian virus 40 large T, can lead to suppression of tumorigenicity of HER-2/neu-overexpressing cancer cells. Here we report that T/t-common, which contains the N-terminal common domain of simian virus 40 large T and small t antigens, could specifically repress the HER-2/neu promoter. When the coding sequence of T/t-common was stably transfected into the HER-2/neu-overexpressing human ovarian carcinoma SK-OV-3 cells, the expression of HER-2/neu was dramatically reduced by the expression of T/t-common. Accordingly the tumorigenic potential of these T/t-common-expressing clones, including the ability to grow anchorage-independently and the ability to induce tumor in nu/nu mice, was also drastically suppressed. Furthermore, when T/t-common was transiently cotransfected with the activated genomic neu into NIH3T3 cells, the transforming activity of the latter was suppressed by T/t-common in soft-agarose microcolony formation assays. Taken together, these data suggest that T/t-common may act as a transformation suppressor of the HER-2/neu oncogene. Oncogene (2000).</description><identifier>ISSN: 0950-9232</identifier><identifier>EISSN: 1476-5594</identifier><identifier>DOI: 10.1038/sj.onc.1203582</identifier><identifier>PMID: 10851070</identifier><identifier>CODEN: ONCNES</identifier><language>eng</language><publisher>England: Nature Publishing Group</publisher><subject>Adenoviruses ; Amino acids ; Animals ; Antigen T (large) ; Antigens ; Antigens, Viral, Tumor - genetics ; Cell Transformation, Neoplastic ; Cell Transformation, Viral ; Chemoresistance ; ErbB protein ; ErbB-2 protein ; Gene Expression Regulation, Neoplastic ; Gene Expression Regulation, Viral ; Genes, erbB-2 ; Genes, Tumor Suppressor ; HER-2 gene ; HER-2/neu gene ; Humans ; Kinases ; Medical prognosis ; Metastases ; Metastasis ; Mice ; neu gene ; Oncogenes ; Ovarian cancer ; Ovarian carcinoma ; Ovaries ; Phosphatase ; Proteins ; simian virus 40 ; Simian virus 40 - genetics ; Tumor Cells, Cultured ; Tumorigenicity ; Tumors ; Viruses</subject><ispartof>Oncogene, 2000-05, Vol.19 (22), p.2704-2713</ispartof><rights>Copyright Nature Publishing Group May 18, 2000</rights><rights>Macmillan Publishers Limited 2000.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c417t-4c3e4e228152cf5ada64b55ff090c7ad13580924c350dd81b7342cb15fff7d423</citedby><cites>FETCH-LOGICAL-c417t-4c3e4e228152cf5ada64b55ff090c7ad13580924c350dd81b7342cb15fff7d423</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27903,27904</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10851070$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lin, Y C</creatorcontrib><creatorcontrib>Peng, J M</creatorcontrib><creatorcontrib>Wang, W B</creatorcontrib><title>The N-terminal common domain of simian virus 40 large T and small t antigens acts as a transformation suppressor of the HER-2/neu oncogene</title><title>Oncogene</title><addtitle>Oncogene</addtitle><description>Overexpression of HER-2/neu (also known as c-erbB-2) proto-oncogene frequently occurs in many different types of human cancers, including ovarian carcinoma, and is known to enhance tumor metastasis and chemoresistance. Previous studies showed that inhibition of HER-2/neu expression by various agents, such as adenovirus E1A and simian virus 40 large T, can lead to suppression of tumorigenicity of HER-2/neu-overexpressing cancer cells. Here we report that T/t-common, which contains the N-terminal common domain of simian virus 40 large T and small t antigens, could specifically repress the HER-2/neu promoter. When the coding sequence of T/t-common was stably transfected into the HER-2/neu-overexpressing human ovarian carcinoma SK-OV-3 cells, the expression of HER-2/neu was dramatically reduced by the expression of T/t-common. Accordingly the tumorigenic potential of these T/t-common-expressing clones, including the ability to grow anchorage-independently and the ability to induce tumor in nu/nu mice, was also drastically suppressed. Furthermore, when T/t-common was transiently cotransfected with the activated genomic neu into NIH3T3 cells, the transforming activity of the latter was suppressed by T/t-common in soft-agarose microcolony formation assays. Taken together, these data suggest that T/t-common may act as a transformation suppressor of the HER-2/neu oncogene. Oncogene (2000).</description><subject>Adenoviruses</subject><subject>Amino acids</subject><subject>Animals</subject><subject>Antigen T (large)</subject><subject>Antigens</subject><subject>Antigens, Viral, Tumor - genetics</subject><subject>Cell Transformation, Neoplastic</subject><subject>Cell Transformation, Viral</subject><subject>Chemoresistance</subject><subject>ErbB protein</subject><subject>ErbB-2 protein</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Gene Expression Regulation, Viral</subject><subject>Genes, erbB-2</subject><subject>Genes, Tumor Suppressor</subject><subject>HER-2 gene</subject><subject>HER-2/neu gene</subject><subject>Humans</subject><subject>Kinases</subject><subject>Medical prognosis</subject><subject>Metastases</subject><subject>Metastasis</subject><subject>Mice</subject><subject>neu gene</subject><subject>Oncogenes</subject><subject>Ovarian cancer</subject><subject>Ovarian carcinoma</subject><subject>Ovaries</subject><subject>Phosphatase</subject><subject>Proteins</subject><subject>simian virus 40</subject><subject>Simian virus 40 - genetics</subject><subject>Tumor Cells, Cultured</subject><subject>Tumorigenicity</subject><subject>Tumors</subject><subject>Viruses</subject><issn>0950-9232</issn><issn>1476-5594</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2000</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>eNqFkUGLFDEQhYMo7uzq1aMEhb31bFU6mXQfZVldYVGQ8dxk0uk1QycZU-kF_4K_2qwzBxFECJU6fPWqeI-xVwhrhLa7ov06RbtGAa3qxBO2Qqk3jVK9fMpW0CtoetGKM3ZOtAcA3YN4zs4QOoWgYcV-br85_qkpLgcfzcxtCiFFPqZgfORp4uSDN5E_-LwQl8Bnk-8d33ITR07BzDMvtS_-3kXixpZa6uMlm0hTysEUX_VoORyyI0r5UbPUnbc3XxpxFd3C6_2pTrsX7NlkZnIvT_8F-_r-Znt929x9_vDx-t1dYyXq0kjbOumE6FAJOykzmo3cKTVN0IPVZsRqBPSiYgrGscOdbqWwO6zEpEcp2gt2edQ95PR9cVSG4Mm6eTbRpYUGjdghQPdfELWSdRVU8O1f4D4tudpJg9hIFNX033Jv_kkJ3QIKxAqtj5DNiSi7aThkH0z-MSAMj4kPtB-qY8Mp8Trw-qS67IIb_8CPEbe_AIMJphw</recordid><startdate>20000518</startdate><enddate>20000518</enddate><creator>Lin, Y C</creator><creator>Peng, J M</creator><creator>Wang, W B</creator><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>Q9U</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20000518</creationdate><title>The N-terminal common domain of simian virus 40 large T and small t antigens acts as a transformation suppressor of the HER-2/neu oncogene</title><author>Lin, Y C ; Peng, J M ; Wang, W B</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c417t-4c3e4e228152cf5ada64b55ff090c7ad13580924c350dd81b7342cb15fff7d423</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2000</creationdate><topic>Adenoviruses</topic><topic>Amino acids</topic><topic>Animals</topic><topic>Antigen T (large)</topic><topic>Antigens</topic><topic>Antigens, Viral, Tumor - 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Academic</collection><jtitle>Oncogene</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lin, Y C</au><au>Peng, J M</au><au>Wang, W B</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The N-terminal common domain of simian virus 40 large T and small t antigens acts as a transformation suppressor of the HER-2/neu oncogene</atitle><jtitle>Oncogene</jtitle><addtitle>Oncogene</addtitle><date>2000-05-18</date><risdate>2000</risdate><volume>19</volume><issue>22</issue><spage>2704</spage><epage>2713</epage><pages>2704-2713</pages><issn>0950-9232</issn><eissn>1476-5594</eissn><coden>ONCNES</coden><abstract>Overexpression of HER-2/neu (also known as c-erbB-2) proto-oncogene frequently occurs in many different types of human cancers, including ovarian carcinoma, and is known to enhance tumor metastasis and chemoresistance. Previous studies showed that inhibition of HER-2/neu expression by various agents, such as adenovirus E1A and simian virus 40 large T, can lead to suppression of tumorigenicity of HER-2/neu-overexpressing cancer cells. Here we report that T/t-common, which contains the N-terminal common domain of simian virus 40 large T and small t antigens, could specifically repress the HER-2/neu promoter. When the coding sequence of T/t-common was stably transfected into the HER-2/neu-overexpressing human ovarian carcinoma SK-OV-3 cells, the expression of HER-2/neu was dramatically reduced by the expression of T/t-common. Accordingly the tumorigenic potential of these T/t-common-expressing clones, including the ability to grow anchorage-independently and the ability to induce tumor in nu/nu mice, was also drastically suppressed. Furthermore, when T/t-common was transiently cotransfected with the activated genomic neu into NIH3T3 cells, the transforming activity of the latter was suppressed by T/t-common in soft-agarose microcolony formation assays. Taken together, these data suggest that T/t-common may act as a transformation suppressor of the HER-2/neu oncogene. Oncogene (2000).</abstract><cop>England</cop><pub>Nature Publishing Group</pub><pmid>10851070</pmid><doi>10.1038/sj.onc.1203582</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adenoviruses Amino acids Animals Antigen T (large) Antigens Antigens, Viral, Tumor - genetics Cell Transformation, Neoplastic Cell Transformation, Viral Chemoresistance ErbB protein ErbB-2 protein Gene Expression Regulation, Neoplastic Gene Expression Regulation, Viral Genes, erbB-2 Genes, Tumor Suppressor HER-2 gene HER-2/neu gene Humans Kinases Medical prognosis Metastases Metastasis Mice neu gene Oncogenes Ovarian cancer Ovarian carcinoma Ovaries Phosphatase Proteins simian virus 40 Simian virus 40 - genetics Tumor Cells, Cultured Tumorigenicity Tumors Viruses |
| title | The N-terminal common domain of simian virus 40 large T and small t antigens acts as a transformation suppressor of the HER-2/neu oncogene |
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