Unmutated proto-src coding region is tumorigenic if expressed from the promoter of Rous sarcoma virus: implications for the gene-mutation hypothesis of cancer
The transforming (onc) genes of oncogenic retroviruses share most or all of their coding sequences with normal cellular genes termed proto-onc genes. The viral genes differ from proto-onc genes in virus-specific promoters and in various point mutations and substitutions of cell-derived coding region...
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| Veröffentlicht in: | Proceedings of the National Academy of Sciences - PNAS 1992-07, Vol.89 (14), p.6393-6397 |
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| creator | Wu, Y. (University of California, Berkeley, CA) Zhou, H Duesberg, P |
| description | The transforming (onc) genes of oncogenic retroviruses share most or all of their coding sequences with normal cellular genes termed proto-onc genes. The viral genes differ from proto-onc genes in virus-specific promoters and in various point mutations and substitutions of cell-derived coding regions. In view of the structural similarities between viral oncogenes and cellular proto-onc genes, the hypothesis has been advanced that proto-onc genes become cellular cancer genes if they have suffered mutations. Indeed, point mutations and substitutions have been observed in the proto-onc genes of some cancers. However, the hypothesis has been difficult to prove because mutated proto-onc genes from tumors do not transform diploid cells. Moreover, owing to the popularity of this hypothesis, even viral oncogenes are thought to derive transforming function from mutations of this cell-derived coding region. A competing hypothesis proposes that enhanced expression from retroviral promoters is necessary and sufficient for oncogenic function of proto-onc genes. To distinguish between these hypotheses we have tested tumorigenicity of RpSV, a synthetic retrovirus with the normal proto-src coding region in a vector derived from Rous sarcoma virus (RSV). In addition, we have tested the role of RSV-specific src point mutations on the tumorigenicity of RpSV. It was found that RpSV with an unmutated proto-src coding region is tumorigenic in chickens and that tumorigenicity is enhanced by RSV-specific src point mutations. It is concluded that retroviral promoters are essential for the transforming function of viral oncogenes and that certain point mutations merely supplement their transforming function. Thus retroviral onc genes are not models for the hypothesis that mutated, but transcriptionally normal, proto-onc genes of certain tumors are cancer genes. |
| doi_str_mv | 10.1073/pnas.89.14.6393 |
| format | Article |
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(University of California, Berkeley, CA) ; Zhou, H ; Duesberg, P</creator><creatorcontrib>Wu, Y. (University of California, Berkeley, CA) ; Zhou, H ; Duesberg, P</creatorcontrib><description>The transforming (onc) genes of oncogenic retroviruses share most or all of their coding sequences with normal cellular genes termed proto-onc genes. The viral genes differ from proto-onc genes in virus-specific promoters and in various point mutations and substitutions of cell-derived coding regions. In view of the structural similarities between viral oncogenes and cellular proto-onc genes, the hypothesis has been advanced that proto-onc genes become cellular cancer genes if they have suffered mutations. Indeed, point mutations and substitutions have been observed in the proto-onc genes of some cancers. However, the hypothesis has been difficult to prove because mutated proto-onc genes from tumors do not transform diploid cells. Moreover, owing to the popularity of this hypothesis, even viral oncogenes are thought to derive transforming function from mutations of this cell-derived coding region. A competing hypothesis proposes that enhanced expression from retroviral promoters is necessary and sufficient for oncogenic function of proto-onc genes. To distinguish between these hypotheses we have tested tumorigenicity of RpSV, a synthetic retrovirus with the normal proto-src coding region in a vector derived from Rous sarcoma virus (RSV). In addition, we have tested the role of RSV-specific src point mutations on the tumorigenicity of RpSV. It was found that RpSV with an unmutated proto-src coding region is tumorigenic in chickens and that tumorigenicity is enhanced by RSV-specific src point mutations. It is concluded that retroviral promoters are essential for the transforming function of viral oncogenes and that certain point mutations merely supplement their transforming function. Thus retroviral onc genes are not models for the hypothesis that mutated, but transcriptionally normal, proto-onc genes of certain tumors are cancer genes.</description><identifier>ISSN: 0027-8424</identifier><identifier>EISSN: 1091-6490</identifier><identifier>DOI: 10.1073/pnas.89.14.6393</identifier><identifier>PMID: 1321438</identifier><identifier>CODEN: PNASA6</identifier><language>eng</language><publisher>Washington, DC: National Academy of Sciences of the United States of America</publisher><subject>Animals ; Avian Sarcoma Viruses - genetics ; Base Sequence ; Biochemistry ; Biological and medical sciences ; Cancer ; Cell physiology ; Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes ; Cell Transformation, Viral ; Chickens ; CODE GENETIQUE ; CODIGO GENETICO ; Codons ; DNA, Recombinant ; DNA, Viral - genetics ; EXPRESION GENICA ; EXPRESSION DES GENES ; Fundamental and applied biological sciences. Psychology ; Gene Expression Regulation, Neoplastic ; Gene Expression Regulation, Viral ; Genes ; Genes, src ; Genetic mutation ; Genetics ; Molecular and cellular biology ; Molecular Sequence Data ; MUTACION ; MUTATION ; NEOPLASMAS ; NEOPLASME ; Oncogenes ; ONCOGENICIDAD ; ONCOGENICITE ; Point mutation ; Promoter regions ; Promoter Regions, Genetic ; Proto-Oncogenes ; Rous sarcoma virus ; Sarcoma ; Sarcoma, Experimental - genetics ; Tumors ; VIRUS DEL SARCOMA DE ROUS ; VIRUS SARCOME DE ROUS ; Viruses</subject><ispartof>Proceedings of the National Academy of Sciences - PNAS, 1992-07, Vol.89 (14), p.6393-6397</ispartof><rights>Copyright 1992 The National Academy of Sciences of the United States of America</rights><rights>1992 INIST-CNRS</rights><rights>Copyright National Academy of Sciences Jul 15, 1992</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c568t-2ea7108da8197fed17a82c359a6fc69801b9d680aa05b44f44d54c816ec4c6093</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Uhttp://www.pnas.org/content/89/14.cover.gif</thumbnail><linktopdf>$$Uhttps://www.jstor.org/stable/pdf/2360016$$EPDF$$P50$$Gjstor$$H</linktopdf><linktohtml>$$Uhttps://www.jstor.org/stable/2360016$$EHTML$$P50$$Gjstor$$H</linktohtml><link.rule.ids>230,314,723,776,780,799,881,27901,27902,53766,53768,57992,58225</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=5445468$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/1321438$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wu, Y. (University of California, Berkeley, CA)</creatorcontrib><creatorcontrib>Zhou, H</creatorcontrib><creatorcontrib>Duesberg, P</creatorcontrib><title>Unmutated proto-src coding region is tumorigenic if expressed from the promoter of Rous sarcoma virus: implications for the gene-mutation hypothesis of cancer</title><title>Proceedings of the National Academy of Sciences - PNAS</title><addtitle>Proc Natl Acad Sci U S A</addtitle><description>The transforming (onc) genes of oncogenic retroviruses share most or all of their coding sequences with normal cellular genes termed proto-onc genes. The viral genes differ from proto-onc genes in virus-specific promoters and in various point mutations and substitutions of cell-derived coding regions. In view of the structural similarities between viral oncogenes and cellular proto-onc genes, the hypothesis has been advanced that proto-onc genes become cellular cancer genes if they have suffered mutations. Indeed, point mutations and substitutions have been observed in the proto-onc genes of some cancers. However, the hypothesis has been difficult to prove because mutated proto-onc genes from tumors do not transform diploid cells. Moreover, owing to the popularity of this hypothesis, even viral oncogenes are thought to derive transforming function from mutations of this cell-derived coding region. A competing hypothesis proposes that enhanced expression from retroviral promoters is necessary and sufficient for oncogenic function of proto-onc genes. To distinguish between these hypotheses we have tested tumorigenicity of RpSV, a synthetic retrovirus with the normal proto-src coding region in a vector derived from Rous sarcoma virus (RSV). In addition, we have tested the role of RSV-specific src point mutations on the tumorigenicity of RpSV. It was found that RpSV with an unmutated proto-src coding region is tumorigenic in chickens and that tumorigenicity is enhanced by RSV-specific src point mutations. It is concluded that retroviral promoters are essential for the transforming function of viral oncogenes and that certain point mutations merely supplement their transforming function. Thus retroviral onc genes are not models for the hypothesis that mutated, but transcriptionally normal, proto-onc genes of certain tumors are cancer genes.</description><subject>Animals</subject><subject>Avian Sarcoma Viruses - genetics</subject><subject>Base Sequence</subject><subject>Biochemistry</subject><subject>Biological and medical sciences</subject><subject>Cancer</subject><subject>Cell physiology</subject><subject>Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes</subject><subject>Cell Transformation, Viral</subject><subject>Chickens</subject><subject>CODE GENETIQUE</subject><subject>CODIGO GENETICO</subject><subject>Codons</subject><subject>DNA, Recombinant</subject><subject>DNA, Viral - genetics</subject><subject>EXPRESION GENICA</subject><subject>EXPRESSION DES GENES</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Gene Expression Regulation, Viral</subject><subject>Genes</subject><subject>Genes, src</subject><subject>Genetic mutation</subject><subject>Genetics</subject><subject>Molecular and cellular biology</subject><subject>Molecular Sequence Data</subject><subject>MUTACION</subject><subject>MUTATION</subject><subject>NEOPLASMAS</subject><subject>NEOPLASME</subject><subject>Oncogenes</subject><subject>ONCOGENICIDAD</subject><subject>ONCOGENICITE</subject><subject>Point mutation</subject><subject>Promoter regions</subject><subject>Promoter Regions, Genetic</subject><subject>Proto-Oncogenes</subject><subject>Rous sarcoma virus</subject><subject>Sarcoma</subject><subject>Sarcoma, Experimental - genetics</subject><subject>Tumors</subject><subject>VIRUS DEL SARCOMA DE ROUS</subject><subject>VIRUS SARCOME DE ROUS</subject><subject>Viruses</subject><issn>0027-8424</issn><issn>1091-6490</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1992</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkl-P1CAUxYnRrOPos4lRQ4zRp85CoRSML2bjv2QTE3WeCUNhhklbukA3u1_GzyrdjrPqgz6RcH7n3MvlAvAYoxVGNTkdehVXXKwwXTEiyB2wwEjgglGB7oIFQmVdcFrS--BBjHuEkKg4OgEnmJSYEr4AP9Z9NyaVTAOH4JMvYtBQ-8b1WxjM1vkeugjT2PngtqZ3GjoLzdUQTIzZY4PvYNqZydz5ZAL0Fn71Y4RRBe07BS9dGOMb6LqhdVqlHBih9eHGlANNcVN-qrO7Hny-jbleDtGq1yY8BPesaqN5dDiXYP3h_fezT8X5l4-fz96dF7piPBWlUTVGvFEci9qaBteKl5pUQjGrmeAIb0TDOFIKVRtKLaVNRTXHzGiqGRJkCd7OucO46UyjTZ-CauUQXKfCtfTKyT-V3u3k1l9KKqr8DUvw6mAP_mI0McnORW3aVvUmD0PWBLG6ZtV_QcxKUeNyaujFX-Dej6HPM5AlwqQWJZrSTmdIBx9jMPbYMEZyWg85rYfkQmIqp_XIjme_v_OWn_ch6y8PuopatTbkX3DxiFWUVpRN2OsDNuX_Um_rSDu2bTJXKZPP_0lm4OkM7GPy4UiUhCGEWZafzLJVXqptyM2sv4k8TsQZ-Qno0_D5</recordid><startdate>19920715</startdate><enddate>19920715</enddate><creator>Wu, Y. 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Psychology</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Gene Expression Regulation, Viral</topic><topic>Genes</topic><topic>Genes, src</topic><topic>Genetic mutation</topic><topic>Genetics</topic><topic>Molecular and cellular biology</topic><topic>Molecular Sequence Data</topic><topic>MUTACION</topic><topic>MUTATION</topic><topic>NEOPLASMAS</topic><topic>NEOPLASME</topic><topic>Oncogenes</topic><topic>ONCOGENICIDAD</topic><topic>ONCOGENICITE</topic><topic>Point mutation</topic><topic>Promoter regions</topic><topic>Promoter Regions, Genetic</topic><topic>Proto-Oncogenes</topic><topic>Rous sarcoma virus</topic><topic>Sarcoma</topic><topic>Sarcoma, Experimental - genetics</topic><topic>Tumors</topic><topic>VIRUS DEL SARCOMA DE ROUS</topic><topic>VIRUS SARCOME DE ROUS</topic><topic>Viruses</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wu, Y. (University of California, Berkeley, CA)</creatorcontrib><creatorcontrib>Zhou, H</creatorcontrib><creatorcontrib>Duesberg, P</creatorcontrib><collection>AGRIS</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>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Ecology Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Proceedings of the National Academy of Sciences - PNAS</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wu, Y. (University of California, Berkeley, CA)</au><au>Zhou, H</au><au>Duesberg, P</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Unmutated proto-src coding region is tumorigenic if expressed from the promoter of Rous sarcoma virus: implications for the gene-mutation hypothesis of cancer</atitle><jtitle>Proceedings of the National Academy of Sciences - PNAS</jtitle><addtitle>Proc Natl Acad Sci U S A</addtitle><date>1992-07-15</date><risdate>1992</risdate><volume>89</volume><issue>14</issue><spage>6393</spage><epage>6397</epage><pages>6393-6397</pages><issn>0027-8424</issn><eissn>1091-6490</eissn><coden>PNASA6</coden><abstract>The transforming (onc) genes of oncogenic retroviruses share most or all of their coding sequences with normal cellular genes termed proto-onc genes. The viral genes differ from proto-onc genes in virus-specific promoters and in various point mutations and substitutions of cell-derived coding regions. In view of the structural similarities between viral oncogenes and cellular proto-onc genes, the hypothesis has been advanced that proto-onc genes become cellular cancer genes if they have suffered mutations. Indeed, point mutations and substitutions have been observed in the proto-onc genes of some cancers. However, the hypothesis has been difficult to prove because mutated proto-onc genes from tumors do not transform diploid cells. Moreover, owing to the popularity of this hypothesis, even viral oncogenes are thought to derive transforming function from mutations of this cell-derived coding region. A competing hypothesis proposes that enhanced expression from retroviral promoters is necessary and sufficient for oncogenic function of proto-onc genes. To distinguish between these hypotheses we have tested tumorigenicity of RpSV, a synthetic retrovirus with the normal proto-src coding region in a vector derived from Rous sarcoma virus (RSV). In addition, we have tested the role of RSV-specific src point mutations on the tumorigenicity of RpSV. It was found that RpSV with an unmutated proto-src coding region is tumorigenic in chickens and that tumorigenicity is enhanced by RSV-specific src point mutations. It is concluded that retroviral promoters are essential for the transforming function of viral oncogenes and that certain point mutations merely supplement their transforming function. Thus retroviral onc genes are not models for the hypothesis that mutated, but transcriptionally normal, proto-onc genes of certain tumors are cancer genes.</abstract><cop>Washington, DC</cop><pub>National Academy of Sciences of the United States of America</pub><pmid>1321438</pmid><doi>10.1073/pnas.89.14.6393</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Proceedings of the National Academy of Sciences - PNAS, 1992-07, Vol.89 (14), p.6393-6397 |
| issn | 0027-8424 1091-6490 |
| language | eng |
| recordid | cdi_pubmed_primary_1321438 |
| source | Jstor Complete Legacy; MEDLINE; PubMed Central; Alma/SFX Local Collection; Free Full-Text Journals in Chemistry |
| subjects | Animals Avian Sarcoma Viruses - genetics Base Sequence Biochemistry Biological and medical sciences Cancer Cell physiology Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes Cell Transformation, Viral Chickens CODE GENETIQUE CODIGO GENETICO Codons DNA, Recombinant DNA, Viral - genetics EXPRESION GENICA EXPRESSION DES GENES Fundamental and applied biological sciences. Psychology Gene Expression Regulation, Neoplastic Gene Expression Regulation, Viral Genes Genes, src Genetic mutation Genetics Molecular and cellular biology Molecular Sequence Data MUTACION MUTATION NEOPLASMAS NEOPLASME Oncogenes ONCOGENICIDAD ONCOGENICITE Point mutation Promoter regions Promoter Regions, Genetic Proto-Oncogenes Rous sarcoma virus Sarcoma Sarcoma, Experimental - genetics Tumors VIRUS DEL SARCOMA DE ROUS VIRUS SARCOME DE ROUS Viruses |
| title | Unmutated proto-src coding region is tumorigenic if expressed from the promoter of Rous sarcoma virus: implications for the gene-mutation hypothesis of cancer |
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