In Vivo Effects of the Epstein–Barr Virus Small RNA EBER-1 on Protein Synthesis and Cell Growth Regulation
Recent studies have suggested a role for the Epstein–Barr virus-encoded RNA EBER-1 in malignant transformation. EBER-1 inhibits the activity of the protein kinase PKR, an inhibitor of protein synthesis with tumour suppressor properties. In human 293 cells and murine embryonic fibroblasts, transient...
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| Veröffentlicht in: | Virology (New York, N.Y.) N.Y.), 2002-06, Vol.297 (2), p.253-269 |
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| container_title | Virology (New York, N.Y.) |
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| creator | Laing, Kenneth G. Elia, Androulla Jeffrey, Ian Matys, Volker Tilleray, Vivienne J. Souberbielle, Bernard Clemens, Michael J. |
| description | Recent studies have suggested a role for the Epstein–Barr virus-encoded RNA EBER-1 in malignant transformation. EBER-1 inhibits the activity of the protein kinase PKR, an inhibitor of protein synthesis with tumour suppressor properties. In human 293 cells and murine embryonic fibroblasts, transient expression of EBER-1 promoted total protein synthesis and enhanced the expression of cotransfected reporter genes. However reporter gene expression was stimulated equally well in cells from control and PKR knockout mice. NIH 3T3 cells stably expressing EBER-1 exhibited a greatly increased frequency of colony formation in soft agar, and protein synthesis in these cells was relatively resistant to inhibition by the calcium ionophore A23187. Nevertheless clones containing a high concentration of EBER-1 were not invariably tumourigenic. We conclude that EBER-1 can enhance protein synthesis by a PKR-independent mechanism and that, although this RNA may contribute to the oncogenic potential of Epstein–Barr virus, its expression is not always sufficient for malignant transformation. |
| doi_str_mv | 10.1006/viro.2002.1354 |
| format | Article |
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EBER-1 inhibits the activity of the protein kinase PKR, an inhibitor of protein synthesis with tumour suppressor properties. In human 293 cells and murine embryonic fibroblasts, transient expression of EBER-1 promoted total protein synthesis and enhanced the expression of cotransfected reporter genes. However reporter gene expression was stimulated equally well in cells from control and PKR knockout mice. NIH 3T3 cells stably expressing EBER-1 exhibited a greatly increased frequency of colony formation in soft agar, and protein synthesis in these cells was relatively resistant to inhibition by the calcium ionophore A23187. Nevertheless clones containing a high concentration of EBER-1 were not invariably tumourigenic. We conclude that EBER-1 can enhance protein synthesis by a PKR-independent mechanism and that, although this RNA may contribute to the oncogenic potential of Epstein–Barr virus, its expression is not always sufficient for malignant transformation.</description><identifier>ISSN: 0042-6822</identifier><identifier>EISSN: 1096-0341</identifier><identifier>DOI: 10.1006/viro.2002.1354</identifier><identifier>PMID: 12083824</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Animals ; Cell Division ; Cell Line ; Cell Line, Transformed ; Cell Transformation, Viral ; EBER-1 RNA ; eIF-2 Kinase - metabolism ; Epstein–Barr virus ; fibroblasts ; Fibroblasts - cytology ; Fibroblasts - metabolism ; Fibroblasts - virology ; Gene Expression Regulation ; growth regulation ; Herpesvirus 4, Human - pathogenicity ; Humans ; malignant transformation ; Mice ; Neoplasms - physiopathology ; Protein Biosynthesis ; protein kinase R ; protein synthesis ; RNA, Viral - physiology ; Transfection ; tumourigenesis</subject><ispartof>Virology (New York, N.Y.), 2002-06, Vol.297 (2), p.253-269</ispartof><rights>2002 Elsevier Science (USA)</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c411t-29b47a61f85a94fe279eac26bf996da427f2861fabeb9e98daecfdadd92fd2e33</citedby><cites>FETCH-LOGICAL-c411t-29b47a61f85a94fe279eac26bf996da427f2861fabeb9e98daecfdadd92fd2e33</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0042682202913541$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65534</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12083824$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Laing, Kenneth G.</creatorcontrib><creatorcontrib>Elia, Androulla</creatorcontrib><creatorcontrib>Jeffrey, Ian</creatorcontrib><creatorcontrib>Matys, Volker</creatorcontrib><creatorcontrib>Tilleray, Vivienne J.</creatorcontrib><creatorcontrib>Souberbielle, Bernard</creatorcontrib><creatorcontrib>Clemens, Michael J.</creatorcontrib><title>In Vivo Effects of the Epstein–Barr Virus Small RNA EBER-1 on Protein Synthesis and Cell Growth Regulation</title><title>Virology (New York, N.Y.)</title><addtitle>Virology</addtitle><description>Recent studies have suggested a role for the Epstein–Barr virus-encoded RNA EBER-1 in malignant transformation. EBER-1 inhibits the activity of the protein kinase PKR, an inhibitor of protein synthesis with tumour suppressor properties. In human 293 cells and murine embryonic fibroblasts, transient expression of EBER-1 promoted total protein synthesis and enhanced the expression of cotransfected reporter genes. However reporter gene expression was stimulated equally well in cells from control and PKR knockout mice. NIH 3T3 cells stably expressing EBER-1 exhibited a greatly increased frequency of colony formation in soft agar, and protein synthesis in these cells was relatively resistant to inhibition by the calcium ionophore A23187. Nevertheless clones containing a high concentration of EBER-1 were not invariably tumourigenic. We conclude that EBER-1 can enhance protein synthesis by a PKR-independent mechanism and that, although this RNA may contribute to the oncogenic potential of Epstein–Barr virus, its expression is not always sufficient for malignant transformation.</description><subject>Animals</subject><subject>Cell Division</subject><subject>Cell Line</subject><subject>Cell Line, Transformed</subject><subject>Cell Transformation, Viral</subject><subject>EBER-1 RNA</subject><subject>eIF-2 Kinase - metabolism</subject><subject>Epstein–Barr virus</subject><subject>fibroblasts</subject><subject>Fibroblasts - cytology</subject><subject>Fibroblasts - metabolism</subject><subject>Fibroblasts - virology</subject><subject>Gene Expression Regulation</subject><subject>growth regulation</subject><subject>Herpesvirus 4, Human - pathogenicity</subject><subject>Humans</subject><subject>malignant transformation</subject><subject>Mice</subject><subject>Neoplasms - physiopathology</subject><subject>Protein Biosynthesis</subject><subject>protein kinase R</subject><subject>protein synthesis</subject><subject>RNA, Viral - physiology</subject><subject>Transfection</subject><subject>tumourigenesis</subject><issn>0042-6822</issn><issn>1096-0341</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkbFu2zAQhomiQeKkWTsWnLrJJSlaIkfbUBMDRhs4TVaCEo8NC1l0SclFtrxD3jBPEgo2kKnIdDjcdz8O9yH0mZIpJaT4tnfBTxkhbErzGf-AJpTIIiM5px_RhBDOskIwdobOY_xDUl-W5BSdUUZELhifoHbV4Xu397iyFpo-Ym9x_wC42sUeXPfy9LzQISQkDBHfbnXb4s2POa4W1Saj2Hf4JvgRxLePXdqLLmLdGbyEBF4F_69_wBv4PbS6d777hE6sbiNcHusFuvte_VpeZ-ufV6vlfJ01nNI-Y7LmpS6oFTMtuQVWStANK2orZWE0Z6VlIo11DbUEKYyGxhptjGTWMMjzC_T1kLsL_u8AsVdbF5t0ku7AD1GVVMwoL_m7IBWcCiJkAqcHsAk-xgBW7YLb6vCoKFGjCDWKUKMINYpIC1-OyUO9BfOGHz-fAHEAID1i7yCo2DjoGjAuJBHKePe_7FeojZiI</recordid><startdate>20020605</startdate><enddate>20020605</enddate><creator>Laing, Kenneth G.</creator><creator>Elia, Androulla</creator><creator>Jeffrey, Ian</creator><creator>Matys, Volker</creator><creator>Tilleray, Vivienne J.</creator><creator>Souberbielle, Bernard</creator><creator>Clemens, Michael J.</creator><general>Elsevier Inc</general><scope>6I.</scope><scope>AAFTH</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>7TM</scope><scope>7U9</scope><scope>H94</scope><scope>7X8</scope></search><sort><creationdate>20020605</creationdate><title>In Vivo Effects of the Epstein–Barr Virus Small RNA EBER-1 on Protein Synthesis and Cell Growth Regulation</title><author>Laing, Kenneth G. ; 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EBER-1 inhibits the activity of the protein kinase PKR, an inhibitor of protein synthesis with tumour suppressor properties. In human 293 cells and murine embryonic fibroblasts, transient expression of EBER-1 promoted total protein synthesis and enhanced the expression of cotransfected reporter genes. However reporter gene expression was stimulated equally well in cells from control and PKR knockout mice. NIH 3T3 cells stably expressing EBER-1 exhibited a greatly increased frequency of colony formation in soft agar, and protein synthesis in these cells was relatively resistant to inhibition by the calcium ionophore A23187. Nevertheless clones containing a high concentration of EBER-1 were not invariably tumourigenic. 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| subjects | Animals Cell Division Cell Line Cell Line, Transformed Cell Transformation, Viral EBER-1 RNA eIF-2 Kinase - metabolism Epstein–Barr virus fibroblasts Fibroblasts - cytology Fibroblasts - metabolism Fibroblasts - virology Gene Expression Regulation growth regulation Herpesvirus 4, Human - pathogenicity Humans malignant transformation Mice Neoplasms - physiopathology Protein Biosynthesis protein kinase R protein synthesis RNA, Viral - physiology Transfection tumourigenesis |
| title | In Vivo Effects of the Epstein–Barr Virus Small RNA EBER-1 on Protein Synthesis and Cell Growth Regulation |
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