RapamycinFungusV1, Main, Exploration, bibRecord, 001779

Immortalization of primary endothelial cells by the K1 protein of Kaposi's sarcoma-associated herpesvirus.

Identifieur interne : 001779 ( Main/Exploration ); précédent : 001778; suivant : 001780

Immortalization of primary endothelial cells by the K1 protein of Kaposi's sarcoma-associated herpesvirus.

Auteurs : Ling Wang [États-Unis] ; Dirk P. Dittmer ; Christine C. Tomlinson ; Farnaz D. Fakhari ; Blossom Damania

Source :

Cancer research [ 0008-5472 ] ; 2006.

RBID : pubmed:16585191

Descripteurs français

English descriptors

KwdEn :
- Animals (MeSH), Cell Survival (physiology), Cell Transformation, Neoplastic (metabolism), Cell Transformation, Neoplastic (pathology), Endothelial Cells (cytology), Endothelial Cells (metabolism), Endothelial Cells (physiology), Enzyme Activation (MeSH), Humans (MeSH), Mice (MeSH), Neoplasms, Experimental (blood supply), Neoplasms, Experimental (metabolism), Neoplasms, Experimental (pathology), Neovascularization, Pathologic (metabolism), Neovascularization, Pathologic (pathology), Phosphatidylinositol 3-Kinases (metabolism), Proto-Oncogene Proteins c-akt (metabolism), Signal Transduction (MeSH), Vascular Endothelial Growth Factor A (metabolism), Vascular Endothelial Growth Factor Receptor-2 (metabolism), Viral Proteins (biosynthesis), Viral Proteins (genetics), Viral Proteins (physiology), src Homology Domains (MeSH).
MESH :
- chemical , biosynthesis : Viral Proteins.
- chemical , genetics : Viral Proteins.
- chemical , metabolism : Phosphatidylinositol 3-Kinases, Proto-Oncogene Proteins c-akt, Vascular Endothelial Growth Factor A, Vascular Endothelial Growth Factor Receptor-2.
- blood supply : Neoplasms, Experimental.
- cytology : Endothelial Cells.
- metabolism : Cell Transformation, Neoplastic, Endothelial Cells, Neoplasms, Experimental, Neovascularization, Pathologic.
- pathology : Cell Transformation, Neoplastic, Neoplasms, Experimental, Neovascularization, Pathologic.
- physiology : Cell Survival, Endothelial Cells, Viral Proteins.
- Animals, Enzyme Activation, Humans, Mice, Signal Transduction, src Homology Domains.

Abstract

Kaposi's sarcoma-associated herpesvirus (KSHV) is linked to three different human cancers: Kaposi's sarcoma, primary effusion lymphoma, and multicentric Castleman's disease. The Kaposi's sarcoma lesion expresses high levels of angiogenic factors and is comprised of a mixed cell population, including endothelial cells that are infected with KSHV. We find that the KSHV K1 protein is expressed in Kaposi's sarcoma lesions and can immortalize and extend the life span of primary human umbilical vein endothelial cells in culture. Vascular endothelial growth factor (VEGF) is critical for the survival of endothelial cells, and we show that expression of K1 in endothelial cells resulted in increased levels of secreted VEGF and the activation of key signaling pathways, including the VEGF/VEGF receptor and the phosphatidylinositol-3'-OH-kinase (PI3K) pathway. The SH2 binding motifs present in the cytoplasmic tail of K1 were critical for K1's ability to activate these pathways. Activation of PI3K by K1 results in activation of Akt kinase and mammalian target of rapamycin and inactivation of the proapoptotic proteins FKHR, glycogen synthase kinase-3, and Bad, which are events indicative of cell survival. Because activation of the PI3K pathway is critical for transformation of many human cells, we suggest that PI3K activation by K1 is involved in endothelial cell immortalization and contributes to KSHV-associated tumorigenesis. We also report that K1 enhances angiogenesis in vivo and increases tumor vasculature and tumor size.

DOI: 10.1158/0008-5472.CAN-05-3680
PubMed: 16585191

Affiliations:

Links toward previous steps (curation, corpus...)

to stream Main, to step Corpus: 001795
to stream Main, to step Curation: 001795

Le document en format XML

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<term>Cell Survival (physiology)</term>
<term>Cell Transformation, Neoplastic (metabolism)</term>
<term>Cell Transformation, Neoplastic (pathology)</term>
<term>Endothelial Cells (cytology)</term>
<term>Endothelial Cells (metabolism)</term>
<term>Endothelial Cells (physiology)</term>
<term>Enzyme Activation (MeSH)</term>
<term>Humans (MeSH)</term>
<term>Mice (MeSH)</term>
<term>Neoplasms, Experimental (blood supply)</term>
<term>Neoplasms, Experimental (metabolism)</term>
<term>Neoplasms, Experimental (pathology)</term>
<term>Neovascularization, Pathologic (metabolism)</term>
<term>Neovascularization, Pathologic (pathology)</term>
<term>Phosphatidylinositol 3-Kinases (metabolism)</term>
<term>Proto-Oncogene Proteins c-akt (metabolism)</term>
<term>Signal Transduction (MeSH)</term>
<term>Vascular Endothelial Growth Factor A (metabolism)</term>
<term>Vascular Endothelial Growth Factor Receptor-2 (metabolism)</term>
<term>Viral Proteins (biosynthesis)</term>
<term>Viral Proteins (genetics)</term>
<term>Viral Proteins (physiology)</term>
<term>src Homology Domains (MeSH)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Activation enzymatique (MeSH)</term>
<term>Animaux (MeSH)</term>
<term>Cellules endothéliales (cytologie)</term>
<term>Cellules endothéliales (métabolisme)</term>
<term>Cellules endothéliales (physiologie)</term>
<term>Domaine d'homologie SRC (MeSH)</term>
<term>Facteur de croissance endothéliale vasculaire de type A (métabolisme)</term>
<term>Humains (MeSH)</term>
<term>Néovascularisation pathologique (anatomopathologie)</term>
<term>Néovascularisation pathologique (métabolisme)</term>
<term>Phosphatidylinositol 3-kinases (métabolisme)</term>
<term>Protéines proto-oncogènes c-akt (métabolisme)</term>
<term>Protéines virales (biosynthèse)</term>
<term>Protéines virales (génétique)</term>
<term>Protéines virales (physiologie)</term>
<term>Récepteur-2 au facteur croissance endothéliale vasculaire (métabolisme)</term>
<term>Souris (MeSH)</term>
<term>Survie cellulaire (physiologie)</term>
<term>Transduction du signal (MeSH)</term>
<term>Transformation cellulaire néoplasique (anatomopathologie)</term>
<term>Transformation cellulaire néoplasique (métabolisme)</term>
<term>Tumeurs expérimentales (anatomopathologie)</term>
<term>Tumeurs expérimentales (métabolisme)</term>
<term>Tumeurs expérimentales (vascularisation)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="biosynthesis" xml:lang="en"><term>Viral Proteins</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Viral Proteins</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Phosphatidylinositol 3-Kinases</term>
<term>Proto-Oncogene Proteins c-akt</term>
<term>Vascular Endothelial Growth Factor A</term>
<term>Vascular Endothelial Growth Factor Receptor-2</term>
</keywords>
<keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Néovascularisation pathologique</term>
<term>Transformation cellulaire néoplasique</term>
<term>Tumeurs expérimentales</term>
</keywords>
<keywords scheme="MESH" qualifier="biosynthèse" xml:lang="fr"><term>Protéines virales</term>
</keywords>
<keywords scheme="MESH" qualifier="blood supply" xml:lang="en"><term>Neoplasms, Experimental</term>
</keywords>
<keywords scheme="MESH" qualifier="cytologie" xml:lang="fr"><term>Cellules endothéliales</term>
</keywords>
<keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>Endothelial Cells</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Protéines virales</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Cell Transformation, Neoplastic</term>
<term>Endothelial Cells</term>
<term>Neoplasms, Experimental</term>
<term>Neovascularization, Pathologic</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Cellules endothéliales</term>
<term>Facteur de croissance endothéliale vasculaire de type A</term>
<term>Néovascularisation pathologique</term>
<term>Phosphatidylinositol 3-kinases</term>
<term>Protéines proto-oncogènes c-akt</term>
<term>Récepteur-2 au facteur croissance endothéliale vasculaire</term>
<term>Transformation cellulaire néoplasique</term>
<term>Tumeurs expérimentales</term>
</keywords>
<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Cell Transformation, Neoplastic</term>
<term>Neoplasms, Experimental</term>
<term>Neovascularization, Pathologic</term>
</keywords>
<keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Cellules endothéliales</term>
<term>Protéines virales</term>
<term>Survie cellulaire</term>
</keywords>
<keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Cell Survival</term>
<term>Endothelial Cells</term>
<term>Viral Proteins</term>
</keywords>
<keywords scheme="MESH" qualifier="vascularisation" xml:lang="fr"><term>Tumeurs expérimentales</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>Enzyme Activation</term>
<term>Humans</term>
<term>Mice</term>
<term>Signal Transduction</term>
<term>src Homology Domains</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Activation enzymatique</term>
<term>Animaux</term>
<term>Domaine d'homologie SRC</term>
<term>Humains</term>
<term>Souris</term>
<term>Transduction du signal</term>
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<front><div type="abstract" xml:lang="en">Kaposi's sarcoma-associated herpesvirus (KSHV) is linked to three different human cancers: Kaposi's sarcoma, primary effusion lymphoma, and multicentric Castleman's disease. The Kaposi's sarcoma lesion expresses high levels of angiogenic factors and is comprised of a mixed cell population, including endothelial cells that are infected with KSHV. We find that the KSHV K1 protein is expressed in Kaposi's sarcoma lesions and can immortalize and extend the life span of primary human umbilical vein endothelial cells in culture. Vascular endothelial growth factor (VEGF) is critical for the survival of endothelial cells, and we show that expression of K1 in endothelial cells resulted in increased levels of secreted VEGF and the activation of key signaling pathways, including the VEGF/VEGF receptor and the phosphatidylinositol-3'-OH-kinase (PI3K) pathway. The SH2 binding motifs present in the cytoplasmic tail of K1 were critical for K1's ability to activate these pathways. Activation of PI3K by K1 results in activation of Akt kinase and mammalian target of rapamycin and inactivation of the proapoptotic proteins FKHR, glycogen synthase kinase-3, and Bad, which are events indicative of cell survival. Because activation of the PI3K pathway is critical for transformation of many human cells, we suggest that PI3K activation by K1 is involved in endothelial cell immortalization and contributes to KSHV-associated tumorigenesis. We also report that K1 enhances angiogenesis in vivo and increases tumor vasculature and tumor size.</div>
</front>
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<DateCompleted><Year>2006</Year>
<Month>05</Month>
<Day>22</Day>
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<DateRevised><Year>2010</Year>
<Month>11</Month>
<Day>18</Day>
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<Month>Apr</Month>
<Day>01</Day>
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<Title>Cancer research</Title>
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<ArticleTitle>Immortalization of primary endothelial cells by the K1 protein of Kaposi's sarcoma-associated herpesvirus.</ArticleTitle>
<Pagination><MedlinePgn>3658-66</MedlinePgn>
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<Abstract><AbstractText>Kaposi's sarcoma-associated herpesvirus (KSHV) is linked to three different human cancers: Kaposi's sarcoma, primary effusion lymphoma, and multicentric Castleman's disease. The Kaposi's sarcoma lesion expresses high levels of angiogenic factors and is comprised of a mixed cell population, including endothelial cells that are infected with KSHV. We find that the KSHV K1 protein is expressed in Kaposi's sarcoma lesions and can immortalize and extend the life span of primary human umbilical vein endothelial cells in culture. Vascular endothelial growth factor (VEGF) is critical for the survival of endothelial cells, and we show that expression of K1 in endothelial cells resulted in increased levels of secreted VEGF and the activation of key signaling pathways, including the VEGF/VEGF receptor and the phosphatidylinositol-3'-OH-kinase (PI3K) pathway. The SH2 binding motifs present in the cytoplasmic tail of K1 were critical for K1's ability to activate these pathways. Activation of PI3K by K1 results in activation of Akt kinase and mammalian target of rapamycin and inactivation of the proapoptotic proteins FKHR, glycogen synthase kinase-3, and Bad, which are events indicative of cell survival. Because activation of the PI3K pathway is critical for transformation of many human cells, we suggest that PI3K activation by K1 is involved in endothelial cell immortalization and contributes to KSHV-associated tumorigenesis. We also report that K1 enhances angiogenesis in vivo and increases tumor vasculature and tumor size.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Wang</LastName>
<ForeName>Ling</ForeName>
<Initials>L</Initials>
<AffiliationInfo><Affiliation>Department of Microbiology and Immunology and Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Dittmer</LastName>
<ForeName>Dirk P</ForeName>
<Initials>DP</Initials>
</Author>
<Author ValidYN="Y"><LastName>Tomlinson</LastName>
<ForeName>Christine C</ForeName>
<Initials>CC</Initials>
</Author>
<Author ValidYN="Y"><LastName>Fakhari</LastName>
<ForeName>Farnaz D</ForeName>
<Initials>FD</Initials>
</Author>
<Author ValidYN="Y"><LastName>Damania</LastName>
<ForeName>Blossom</ForeName>
<Initials>B</Initials>
</Author>
</AuthorList>
<Language>eng</Language>
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<Agency>NCI NIH HHS</Agency>
<Country>United States</Country>
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<Acronym>CA</Acronym>
<Agency>NCI NIH HHS</Agency>
<Country>United States</Country>
</Grant>
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<Country>United States</Country>
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<ChemicalList><Chemical><RegistryNumber>0</RegistryNumber>
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<Chemical><RegistryNumber>0</RegistryNumber>
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<Chemical><RegistryNumber>EC 2.7.10.1</RegistryNumber>
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<Chemical><RegistryNumber>EC 2.7.11.1</RegistryNumber>
<NameOfSubstance UI="D051057">Proto-Oncogene Proteins c-akt</NameOfSubstance>
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<CitationSubset>IM</CitationSubset>
<MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName>
</MeshHeading>
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<QualifierName UI="Q000473" MajorTopicYN="Y">pathology</QualifierName>
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<MeshHeading><DescriptorName UI="D042783" MajorTopicYN="N">Endothelial Cells</DescriptorName>
<QualifierName UI="Q000166" MajorTopicYN="Y">cytology</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
<QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName>
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<MeshHeading><DescriptorName UI="D004789" MajorTopicYN="N">Enzyme Activation</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName>
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<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
<QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D009389" MajorTopicYN="N">Neovascularization, Pathologic</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
<QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D019869" MajorTopicYN="N">Phosphatidylinositol 3-Kinases</DescriptorName>
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</MeshHeading>
<MeshHeading><DescriptorName UI="D051057" MajorTopicYN="N">Proto-Oncogene Proteins c-akt</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D042461" MajorTopicYN="N">Vascular Endothelial Growth Factor A</DescriptorName>
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<MeshHeading><DescriptorName UI="D040301" MajorTopicYN="N">Vascular Endothelial Growth Factor Receptor-2</DescriptorName>
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<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D018909" MajorTopicYN="N">src Homology Domains</DescriptorName>
</MeshHeading>
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<Month>4</Month>
<Day>6</Day>
<Hour>9</Hour>
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<affiliations><list><country><li>États-Unis</li>
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<region><li>Caroline du Nord</li>
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<settlement><li>Chapel Hill (Caroline du Nord)</li>
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<orgName><li>Université de Caroline du Nord à Chapel Hill</li>
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</list>
<tree><noCountry><name sortKey="Damania, Blossom" sort="Damania, Blossom" uniqKey="Damania B" first="Blossom" last="Damania">Blossom Damania</name>
<name sortKey="Dittmer, Dirk P" sort="Dittmer, Dirk P" uniqKey="Dittmer D" first="Dirk P" last="Dittmer">Dirk P. Dittmer</name>
<name sortKey="Fakhari, Farnaz D" sort="Fakhari, Farnaz D" uniqKey="Fakhari F" first="Farnaz D" last="Fakhari">Farnaz D. Fakhari</name>
<name sortKey="Tomlinson, Christine C" sort="Tomlinson, Christine C" uniqKey="Tomlinson C" first="Christine C" last="Tomlinson">Christine C. Tomlinson</name>
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<country name="États-Unis"><region name="Caroline du Nord"><name sortKey="Wang, Ling" sort="Wang, Ling" uniqKey="Wang L" first="Ling" last="Wang">Ling Wang</name>
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{{Explor lien
   |wiki=    Bois
   |area=    RapamycinFungusV1
   |flux=    Main
   |étape=   Exploration
   |type=    RBID
   |clé=     pubmed:16585191
   |texte=   Immortalization of primary endothelial cells by the K1 protein of Kaposi's sarcoma-associated herpesvirus.
}}

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	Serveur d'exploration sur la rapamycine et les champignons
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Serveur d'exploration sur la rapamycine et les champignons

Immortalization of primary endothelial cells by the K1 protein of Kaposi's sarcoma-associated herpesvirus.

Immortalization of primary endothelial cells by the K1 protein of Kaposi's sarcoma-associated herpesvirus.

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