Reduced skin tumor development in cyclin D1-deficient mice highlights the oncogenic ras pathway in vivo
Cyclin D1 is part of a cell cycle control node consistently deregulated in most human cancers. However, studies with cyclin D1-null mice indicate that it is dispensable for normal mouse development as well as cell growth in culture. Here, we provide evidence that ras-mediated tumorigenesis depends o...
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| Veröffentlicht in: | Genes & development 1998-08, Vol.12 (16), p.2469-2474 |
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| container_title | Genes & development |
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| creator | Robles, A I Rodriguez-Puebla, M L Glick, A B Trempus, C Hansen, L Sicinski, P Tennant, R W Weinberg, R A Yuspa, S H Conti, C J |
| description | Cyclin D1 is part of a cell cycle control node consistently deregulated in most human cancers. However, studies with cyclin D1-null mice indicate that it is dispensable for normal mouse development as well as cell growth in culture. Here, we provide evidence that ras-mediated tumorigenesis depends on signaling pathways that act preferentially through cyclin D1. Cyclin D1 expression and the activity of its associated kinase are up-regulated in keratinocytes in response to oncogenic ras. Furthermore, cyclin D1 deficiency results in up to an 80% decrease in the development of squamous tumors generated through either grafting of retroviral ras-transduced keratinocytes, phorbol ester treatment of ras transgenic mice, or two-stage carcinogenesis. |
| doi_str_mv | 10.1101/gad.12.16.2469 |
| format | Article |
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However, studies with cyclin D1-null mice indicate that it is dispensable for normal mouse development as well as cell growth in culture. Here, we provide evidence that ras-mediated tumorigenesis depends on signaling pathways that act preferentially through cyclin D1. Cyclin D1 expression and the activity of its associated kinase are up-regulated in keratinocytes in response to oncogenic ras. Furthermore, cyclin D1 deficiency results in up to an 80% decrease in the development of squamous tumors generated through either grafting of retroviral ras-transduced keratinocytes, phorbol ester treatment of ras transgenic mice, or two-stage carcinogenesis.</description><identifier>ISSN: 0890-9369</identifier><identifier>EISSN: 1549-5477</identifier><identifier>DOI: 10.1101/gad.12.16.2469</identifier><identifier>PMID: 9716400</identifier><language>eng</language><publisher>United States: Cold Spring Harbor Laboratory Press</publisher><subject>Animals ; Cell Transformation, Neoplastic ; Cyclin D1 - deficiency ; Cyclin D1 - genetics ; Cyclin D1 - physiology ; Cyclin E - genetics ; Cyclin-Dependent Kinase 4 ; Cyclin-Dependent Kinases - metabolism ; Genes, ras - physiology ; Humans ; Keratinocytes - metabolism ; Mice ; Mice, Transgenic ; Proto-Oncogene Proteins ; Research Communication ; Retroviridae - genetics ; Skin Neoplasms - genetics ; Skin Neoplasms - physiopathology</subject><ispartof>Genes & development, 1998-08, Vol.12 (16), p.2469-2474</ispartof><rights>Copyright © 1998, Cold Spring Harbor Laboratory Press 1998</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c481t-656939ab7b4bf1f30d0c90b26e7447423aaed561fc81c473ae4b46c31d2306863</citedby><cites>FETCH-LOGICAL-c481t-656939ab7b4bf1f30d0c90b26e7447423aaed561fc81c473ae4b46c31d2306863</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC317082/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC317082/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9716400$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Robles, A I</creatorcontrib><creatorcontrib>Rodriguez-Puebla, M L</creatorcontrib><creatorcontrib>Glick, A B</creatorcontrib><creatorcontrib>Trempus, C</creatorcontrib><creatorcontrib>Hansen, L</creatorcontrib><creatorcontrib>Sicinski, P</creatorcontrib><creatorcontrib>Tennant, R W</creatorcontrib><creatorcontrib>Weinberg, R A</creatorcontrib><creatorcontrib>Yuspa, S H</creatorcontrib><creatorcontrib>Conti, C J</creatorcontrib><title>Reduced skin tumor development in cyclin D1-deficient mice highlights the oncogenic ras pathway in vivo</title><title>Genes & development</title><addtitle>Genes Dev</addtitle><description>Cyclin D1 is part of a cell cycle control node consistently deregulated in most human cancers. However, studies with cyclin D1-null mice indicate that it is dispensable for normal mouse development as well as cell growth in culture. Here, we provide evidence that ras-mediated tumorigenesis depends on signaling pathways that act preferentially through cyclin D1. Cyclin D1 expression and the activity of its associated kinase are up-regulated in keratinocytes in response to oncogenic ras. Furthermore, cyclin D1 deficiency results in up to an 80% decrease in the development of squamous tumors generated through either grafting of retroviral ras-transduced keratinocytes, phorbol ester treatment of ras transgenic mice, or two-stage carcinogenesis.</description><subject>Animals</subject><subject>Cell Transformation, Neoplastic</subject><subject>Cyclin D1 - deficiency</subject><subject>Cyclin D1 - genetics</subject><subject>Cyclin D1 - physiology</subject><subject>Cyclin E - genetics</subject><subject>Cyclin-Dependent Kinase 4</subject><subject>Cyclin-Dependent Kinases - metabolism</subject><subject>Genes, ras - physiology</subject><subject>Humans</subject><subject>Keratinocytes - metabolism</subject><subject>Mice</subject><subject>Mice, Transgenic</subject><subject>Proto-Oncogene Proteins</subject><subject>Research Communication</subject><subject>Retroviridae - genetics</subject><subject>Skin Neoplasms - genetics</subject><subject>Skin Neoplasms - physiopathology</subject><issn>0890-9369</issn><issn>1549-5477</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1998</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVUcFq3DAUFCUl3aS99lbQqTc7epZWsg49lKRNAoFAac9Clp5ttba1tewN-_fVkiU0h8fAezPzBoaQj8BKAAZXnfUlVCXIshJSvyEb2ApdbIVSZ2TDas0KzaV-Ry5S-s0Yk0zKc3KuFUjB2IZ0P9CvDj1Nf8JEl3WMM_W4xyHuRpwWmpfu4IYMN1B4bIMLx_UYHNI-dP2QZ0l06ZHGycUOp-DobBPd2aV_soejwT7s43vytrVDwg8nvCS_vn_7eX1XPDze3l9_fSicqGEp5FZqrm2jGtG00HLmmdOsqSQqIZSouLXotxJaV4MTilsUjZCOg684k7Xkl-TLs-9ubUb0Loed7WB2cxjtfDDRBvP6MoXedHFvOChWV1n_-aSf498V02LGkBwOg50wrslATsgU55lYPhPdHFOasX35AcwcmzG5GQNVVphjM1nw6f9kL_RTFfwfQYOL7Q</recordid><startdate>19980815</startdate><enddate>19980815</enddate><creator>Robles, A I</creator><creator>Rodriguez-Puebla, M L</creator><creator>Glick, A B</creator><creator>Trempus, C</creator><creator>Hansen, L</creator><creator>Sicinski, P</creator><creator>Tennant, R W</creator><creator>Weinberg, R A</creator><creator>Yuspa, S H</creator><creator>Conti, C J</creator><general>Cold Spring Harbor Laboratory Press</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>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope><scope>5PM</scope></search><sort><creationdate>19980815</creationdate><title>Reduced skin tumor development in cyclin D1-deficient mice highlights the oncogenic ras pathway in vivo</title><author>Robles, A I ; Rodriguez-Puebla, M L ; Glick, A B ; Trempus, C ; Hansen, L ; Sicinski, P ; Tennant, R W ; Weinberg, R A ; Yuspa, S H ; Conti, C J</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c481t-656939ab7b4bf1f30d0c90b26e7447423aaed561fc81c473ae4b46c31d2306863</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1998</creationdate><topic>Animals</topic><topic>Cell Transformation, Neoplastic</topic><topic>Cyclin D1 - deficiency</topic><topic>Cyclin D1 - genetics</topic><topic>Cyclin D1 - physiology</topic><topic>Cyclin E - genetics</topic><topic>Cyclin-Dependent Kinase 4</topic><topic>Cyclin-Dependent Kinases - metabolism</topic><topic>Genes, ras - physiology</topic><topic>Humans</topic><topic>Keratinocytes - metabolism</topic><topic>Mice</topic><topic>Mice, Transgenic</topic><topic>Proto-Oncogene Proteins</topic><topic>Research Communication</topic><topic>Retroviridae - genetics</topic><topic>Skin Neoplasms - genetics</topic><topic>Skin Neoplasms - physiopathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Robles, A I</creatorcontrib><creatorcontrib>Rodriguez-Puebla, M L</creatorcontrib><creatorcontrib>Glick, A B</creatorcontrib><creatorcontrib>Trempus, C</creatorcontrib><creatorcontrib>Hansen, L</creatorcontrib><creatorcontrib>Sicinski, P</creatorcontrib><creatorcontrib>Tennant, R W</creatorcontrib><creatorcontrib>Weinberg, R A</creatorcontrib><creatorcontrib>Yuspa, S H</creatorcontrib><creatorcontrib>Conti, C J</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Genes & development</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Robles, A I</au><au>Rodriguez-Puebla, M L</au><au>Glick, A B</au><au>Trempus, C</au><au>Hansen, L</au><au>Sicinski, P</au><au>Tennant, R W</au><au>Weinberg, R A</au><au>Yuspa, S H</au><au>Conti, C J</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Reduced skin tumor development in cyclin D1-deficient mice highlights the oncogenic ras pathway in vivo</atitle><jtitle>Genes & development</jtitle><addtitle>Genes Dev</addtitle><date>1998-08-15</date><risdate>1998</risdate><volume>12</volume><issue>16</issue><spage>2469</spage><epage>2474</epage><pages>2469-2474</pages><issn>0890-9369</issn><eissn>1549-5477</eissn><abstract>Cyclin D1 is part of a cell cycle control node consistently deregulated in most human cancers. However, studies with cyclin D1-null mice indicate that it is dispensable for normal mouse development as well as cell growth in culture. Here, we provide evidence that ras-mediated tumorigenesis depends on signaling pathways that act preferentially through cyclin D1. Cyclin D1 expression and the activity of its associated kinase are up-regulated in keratinocytes in response to oncogenic ras. Furthermore, cyclin D1 deficiency results in up to an 80% decrease in the development of squamous tumors generated through either grafting of retroviral ras-transduced keratinocytes, phorbol ester treatment of ras transgenic mice, or two-stage carcinogenesis.</abstract><cop>United States</cop><pub>Cold Spring Harbor Laboratory Press</pub><pmid>9716400</pmid><doi>10.1101/gad.12.16.2469</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Cell Transformation, Neoplastic Cyclin D1 - deficiency Cyclin D1 - genetics Cyclin D1 - physiology Cyclin E - genetics Cyclin-Dependent Kinase 4 Cyclin-Dependent Kinases - metabolism Genes, ras - physiology Humans Keratinocytes - metabolism Mice Mice, Transgenic Proto-Oncogene Proteins Research Communication Retroviridae - genetics Skin Neoplasms - genetics Skin Neoplasms - physiopathology |
| title | Reduced skin tumor development in cyclin D1-deficient mice highlights the oncogenic ras pathway in vivo |
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