RapamycinFungusV1, Main, Exploration, bibRecord, 000667

Activation of sterol regulatory element-binding protein 1 (SREBP1)-mediated lipogenesis by the Epstein-Barr virus-encoded latent membrane protein 1 (LMP1) promotes cell proliferation and progression of nasopharyngeal carcinoma.

Identifieur interne : 000667 ( Main/Exploration ); précédent : 000666; suivant : 000668

Activation of sterol regulatory element-binding protein 1 (SREBP1)-mediated lipogenesis by the Epstein-Barr virus-encoded latent membrane protein 1 (LMP1) promotes cell proliferation and progression of nasopharyngeal carcinoma.

Auteurs : Angela Kwok-Fung Lo [Hong Kong] ; Raymond Wai-Ming Lung [Hong Kong] ; Christopher W. Dawson [Royaume-Uni] ; Lawrence S. Young [Royaume-Uni] ; Chuen-Wai Ko [Hong Kong] ; Walter Wai Yeung [Hong Kong] ; Wei Kang [Hong Kong] ; Ka-Fai To [Hong Kong] ; Kwok-Wai Lo [Hong Kong]

Source :

The Journal of pathology [ 1096-9896 ] ; 2018.

RBID : pubmed:29968360

Descripteurs français

English descriptors

KwdEn :
- Animals (MeSH), Antineoplastic Agents (pharmacology), Cell Line, Tumor (MeSH), Cell Proliferation (drug effects), Disease Progression (MeSH), Fatty Acid Synthase, Type I (genetics), Fatty Acid Synthase, Type I (metabolism), Female (MeSH), Herpesvirus 4, Human (genetics), Herpesvirus 4, Human (metabolism), Humans (MeSH), Lipid Droplets (metabolism), Lipogenesis (drug effects), Luteolin (pharmacology), Male (MeSH), Mice, Inbred BALB C (MeSH), Mice, Nude (MeSH), Middle Aged (MeSH), Naphthyridines (pharmacology), Nasopharyngeal Carcinoma (drug therapy), Nasopharyngeal Carcinoma (metabolism), Nasopharyngeal Carcinoma (pathology), Nasopharyngeal Carcinoma (virology), Nasopharyngeal Neoplasms (drug therapy), Nasopharyngeal Neoplasms (metabolism), Nasopharyngeal Neoplasms (pathology), Nasopharyngeal Neoplasms (virology), Pyridines (pharmacology), Signal Transduction (MeSH), Sterol Regulatory Element Binding Protein 1 (genetics), Sterol Regulatory Element Binding Protein 1 (metabolism), TOR Serine-Threonine Kinases (antagonists & inhibitors), TOR Serine-Threonine Kinases (genetics), TOR Serine-Threonine Kinases (metabolism), Thiazoles (pharmacology), Viral Matrix Proteins (genetics), Viral Matrix Proteins (metabolism), Xenograft Model Antitumor Assays (MeSH).
MESH :
- chemical , antagonists & inhibitors : TOR Serine-Threonine Kinases.
- chemical , genetics : Fatty Acid Synthase, Type I, Sterol Regulatory Element Binding Protein 1, TOR Serine-Threonine Kinases, Viral Matrix Proteins.
- chemical , metabolism : Fatty Acid Synthase, Type I, Sterol Regulatory Element Binding Protein 1, TOR Serine-Threonine Kinases, Viral Matrix Proteins.
- chemical , pharmacology : Antineoplastic Agents, Luteolin, Naphthyridines, Pyridines, Thiazoles.
- drug effects : Cell Proliferation, Lipogenesis.
- drug therapy : Nasopharyngeal Carcinoma, Nasopharyngeal Neoplasms.
- genetics : Herpesvirus 4, Human.
- metabolism : Herpesvirus 4, Human, Lipid Droplets, Nasopharyngeal Carcinoma, Nasopharyngeal Neoplasms.
- pathology : Nasopharyngeal Carcinoma, Nasopharyngeal Neoplasms.
- virology : Nasopharyngeal Carcinoma, Nasopharyngeal Neoplasms.
- Animals, Cell Line, Tumor, Disease Progression, Female, Humans, Male, Mice, Inbred BALB C, Mice, Nude, Middle Aged, Signal Transduction, Xenograft Model Antitumor Assays.

Abstract

Nasopharyngeal carcinoma (NPC) is closely associated with Epstein-Barr virus (EBV) infection. The EBV-encoded latent membrane protein 1 (LMP1), which is commonly expressed in NPC, engages multiple signaling pathways that promote cell growth, transformation, and metabolic reprogramming. Here, we report a novel function of LMP1 in promoting de novo lipogenesis. LMP1 increases the expression, maturation and activation of sterol regulatory element-binding protein 1 (SREBP1), a master regulator of lipogenesis, and its downstream target fatty acid synthase (FASN). LMP1 also induces de novo lipid synthesis and lipid droplet formation. In contrast, small interfering RNA (siRNA) knockdown of LMP1 in EBV-infected epithelial cells diminished SREBP1 activation and lipid biosynthesis. Furthermore, inhibition of the mammalian target of rapamycin (mTOR) pathway, through the use of either mTOR inhibitors or siRNAs, significantly reduced LMP1-mediated SREBP1 activity and lipogenesis, indicating that LMP1 activation of the mTOR pathway is required for SREBP1-mediated lipogenesis. In primary NPC tumors, FASN overexpression is common, with high levels correlating significantly with LMP1 expression. Moreover, elevated FASN expression was associated with aggressive disease and poor survival in NPC patients. Luteolin and fatostatin, two inhibitors of lipogenesis, suppressed lipogenesis and proliferation of nasopharyngeal epithelial cells, effects that were more profound in cells expressing LMP1. Luteolin and fatostatin also dramatically inhibited NPC tumor growth in vitro and in vivo. Our findings demonstrate that LMP1 activation of SREBP1-mediated lipogenesis promotes tumor cell growth and is involved in EBV-driven NPC pathogenesis. Our results also reveal the therapeutic potential of utilizing lipogenesis inhibitors in the treatment of locally advanced or metastatic NPC. © 2018 The Authors. The Journal of Pathology published by John Wiley & Sons Ltd on behalf of Pathological Society of Great Britain and Ireland.

DOI: 10.1002/path.5130
PubMed: 29968360
PubMed Central: PMC6175466

Affiliations:

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

to stream Main, to step Corpus: 000513
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Le document en format XML

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<sourceDesc><biblStruct><analytic><title xml:lang="en">Activation of sterol regulatory element-binding protein 1 (SREBP1)-mediated lipogenesis by the Epstein-Barr virus-encoded latent membrane protein 1 (LMP1) promotes cell proliferation and progression of nasopharyngeal carcinoma.</title>
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<term>Antineoplastic Agents (pharmacology)</term>
<term>Cell Line, Tumor (MeSH)</term>
<term>Cell Proliferation (drug effects)</term>
<term>Disease Progression (MeSH)</term>
<term>Fatty Acid Synthase, Type I (genetics)</term>
<term>Fatty Acid Synthase, Type I (metabolism)</term>
<term>Female (MeSH)</term>
<term>Herpesvirus 4, Human (genetics)</term>
<term>Herpesvirus 4, Human (metabolism)</term>
<term>Humans (MeSH)</term>
<term>Lipid Droplets (metabolism)</term>
<term>Lipogenesis (drug effects)</term>
<term>Luteolin (pharmacology)</term>
<term>Male (MeSH)</term>
<term>Mice, Inbred BALB C (MeSH)</term>
<term>Mice, Nude (MeSH)</term>
<term>Middle Aged (MeSH)</term>
<term>Naphthyridines (pharmacology)</term>
<term>Nasopharyngeal Carcinoma (drug therapy)</term>
<term>Nasopharyngeal Carcinoma (metabolism)</term>
<term>Nasopharyngeal Carcinoma (pathology)</term>
<term>Nasopharyngeal Carcinoma (virology)</term>
<term>Nasopharyngeal Neoplasms (drug therapy)</term>
<term>Nasopharyngeal Neoplasms (metabolism)</term>
<term>Nasopharyngeal Neoplasms (pathology)</term>
<term>Nasopharyngeal Neoplasms (virology)</term>
<term>Pyridines (pharmacology)</term>
<term>Signal Transduction (MeSH)</term>
<term>Sterol Regulatory Element Binding Protein 1 (genetics)</term>
<term>Sterol Regulatory Element Binding Protein 1 (metabolism)</term>
<term>TOR Serine-Threonine Kinases (antagonists & inhibitors)</term>
<term>TOR Serine-Threonine Kinases (genetics)</term>
<term>TOR Serine-Threonine Kinases (metabolism)</term>
<term>Thiazoles (pharmacology)</term>
<term>Viral Matrix Proteins (genetics)</term>
<term>Viral Matrix Proteins (metabolism)</term>
<term>Xenograft Model Antitumor Assays (MeSH)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Adulte d'âge moyen (MeSH)</term>
<term>Animaux (MeSH)</term>
<term>Antinéoplasiques (pharmacologie)</term>
<term>Cancer du nasopharynx (anatomopathologie)</term>
<term>Cancer du nasopharynx (métabolisme)</term>
<term>Cancer du nasopharynx (traitement médicamenteux)</term>
<term>Cancer du nasopharynx (virologie)</term>
<term>Fatty acid synthase type I (génétique)</term>
<term>Fatty acid synthase type I (métabolisme)</term>
<term>Femelle (MeSH)</term>
<term>Gouttelettes lipidiques (métabolisme)</term>
<term>Herpèsvirus humain de type 4 (génétique)</term>
<term>Herpèsvirus humain de type 4 (métabolisme)</term>
<term>Humains (MeSH)</term>
<term>Lignée cellulaire tumorale (MeSH)</term>
<term>Lipogenèse (effets des médicaments et des substances chimiques)</term>
<term>Lutéoline (pharmacologie)</term>
<term>Mâle (MeSH)</term>
<term>Naphtyridines (pharmacologie)</term>
<term>Prolifération cellulaire (effets des médicaments et des substances chimiques)</term>
<term>Protéine-1 de liaison à l'élément de régulation des stérols (génétique)</term>
<term>Protéine-1 de liaison à l'élément de régulation des stérols (métabolisme)</term>
<term>Protéines de la matrice virale (génétique)</term>
<term>Protéines de la matrice virale (métabolisme)</term>
<term>Pyridines (pharmacologie)</term>
<term>Souris de lignée BALB C (MeSH)</term>
<term>Souris nude (MeSH)</term>
<term>Sérine-thréonine kinases TOR (antagonistes et inhibiteurs)</term>
<term>Sérine-thréonine kinases TOR (génétique)</term>
<term>Sérine-thréonine kinases TOR (métabolisme)</term>
<term>Tests d'activité antitumorale sur modèle de xénogreffe (MeSH)</term>
<term>Thiazoles (pharmacologie)</term>
<term>Transduction du signal (MeSH)</term>
<term>Tumeurs du rhinopharynx (anatomopathologie)</term>
<term>Tumeurs du rhinopharynx (métabolisme)</term>
<term>Tumeurs du rhinopharynx (traitement médicamenteux)</term>
<term>Tumeurs du rhinopharynx (virologie)</term>
<term>Évolution de la maladie (MeSH)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en"><term>TOR Serine-Threonine Kinases</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Fatty Acid Synthase, Type I</term>
<term>Sterol Regulatory Element Binding Protein 1</term>
<term>TOR Serine-Threonine Kinases</term>
<term>Viral Matrix Proteins</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Fatty Acid Synthase, Type I</term>
<term>Sterol Regulatory Element Binding Protein 1</term>
<term>TOR Serine-Threonine Kinases</term>
<term>Viral Matrix Proteins</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Antineoplastic Agents</term>
<term>Luteolin</term>
<term>Naphthyridines</term>
<term>Pyridines</term>
<term>Thiazoles</term>
</keywords>
<keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Cancer du nasopharynx</term>
<term>Tumeurs du rhinopharynx</term>
</keywords>
<keywords scheme="MESH" qualifier="antagonistes et inhibiteurs" xml:lang="fr"><term>Sérine-thréonine kinases TOR</term>
</keywords>
<keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Cell Proliferation</term>
<term>Lipogenesis</term>
</keywords>
<keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Nasopharyngeal Carcinoma</term>
<term>Nasopharyngeal Neoplasms</term>
</keywords>
<keywords scheme="MESH" qualifier="effets des médicaments et des substances chimiques" xml:lang="fr"><term>Lipogenèse</term>
<term>Prolifération cellulaire</term>
</keywords>
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</keywords>
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<term>Herpèsvirus humain de type 4</term>
<term>Protéine-1 de liaison à l'élément de régulation des stérols</term>
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<term>Sérine-thréonine kinases TOR</term>
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<term>Nasopharyngeal Carcinoma</term>
<term>Nasopharyngeal Neoplasms</term>
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<term>Herpèsvirus humain de type 4</term>
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<term>Protéines de la matrice virale</term>
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<term>Tumeurs du rhinopharynx</term>
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<term>Naphtyridines</term>
<term>Pyridines</term>
<term>Thiazoles</term>
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<term>Nasopharyngeal Neoplasms</term>
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<term>Cell Line, Tumor</term>
<term>Disease Progression</term>
<term>Female</term>
<term>Humans</term>
<term>Male</term>
<term>Mice, Inbred BALB C</term>
<term>Mice, Nude</term>
<term>Middle Aged</term>
<term>Signal Transduction</term>
<term>Xenograft Model Antitumor Assays</term>
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<term>Femelle</term>
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<term>Lignée cellulaire tumorale</term>
<term>Mâle</term>
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<term>Souris nude</term>
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<front><div type="abstract" xml:lang="en">Nasopharyngeal carcinoma (NPC) is closely associated with Epstein-Barr virus (EBV) infection. The EBV-encoded latent membrane protein 1 (LMP1), which is commonly expressed in NPC, engages multiple signaling pathways that promote cell growth, transformation, and metabolic reprogramming. Here, we report a novel function of LMP1 in promoting de novo lipogenesis. LMP1 increases the expression, maturation and activation of sterol regulatory element-binding protein 1 (SREBP1), a master regulator of lipogenesis, and its downstream target fatty acid synthase (FASN). LMP1 also induces de novo lipid synthesis and lipid droplet formation. In contrast, small interfering RNA (siRNA) knockdown of LMP1 in EBV-infected epithelial cells diminished SREBP1 activation and lipid biosynthesis. Furthermore, inhibition of the mammalian target of rapamycin (mTOR) pathway, through the use of either mTOR inhibitors or siRNAs, significantly reduced LMP1-mediated SREBP1 activity and lipogenesis, indicating that LMP1 activation of the mTOR pathway is required for SREBP1-mediated lipogenesis. In primary NPC tumors, FASN overexpression is common, with high levels correlating significantly with LMP1 expression. Moreover, elevated FASN expression was associated with aggressive disease and poor survival in NPC patients. Luteolin and fatostatin, two inhibitors of lipogenesis, suppressed lipogenesis and proliferation of nasopharyngeal epithelial cells, effects that were more profound in cells expressing LMP1. Luteolin and fatostatin also dramatically inhibited NPC tumor growth in vitro and in vivo. Our findings demonstrate that LMP1 activation of SREBP1-mediated lipogenesis promotes tumor cell growth and is involved in EBV-driven NPC pathogenesis. Our results also reveal the therapeutic potential of utilizing lipogenesis inhibitors in the treatment of locally advanced or metastatic NPC. © 2018 The Authors. The Journal of Pathology published by John Wiley & Sons Ltd on behalf of Pathological Society of Great Britain and Ireland.</div>
</front>
</TEI>
<pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">29968360</PMID>
<DateCompleted><Year>2019</Year>
<Month>10</Month>
<Day>22</Day>
</DateCompleted>
<DateRevised><Year>2019</Year>
<Month>10</Month>
<Day>22</Day>
</DateRevised>
<Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1096-9896</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>246</Volume>
<Issue>2</Issue>
<PubDate><Year>2018</Year>
<Month>10</Month>
</PubDate>
</JournalIssue>
<Title>The Journal of pathology</Title>
<ISOAbbreviation>J Pathol</ISOAbbreviation>
</Journal>
<ArticleTitle>Activation of sterol regulatory element-binding protein 1 (SREBP1)-mediated lipogenesis by the Epstein-Barr virus-encoded latent membrane protein 1 (LMP1) promotes cell proliferation and progression of nasopharyngeal carcinoma.</ArticleTitle>
<Pagination><MedlinePgn>180-190</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.1002/path.5130</ELocationID>
<Abstract><AbstractText>Nasopharyngeal carcinoma (NPC) is closely associated with Epstein-Barr virus (EBV) infection. The EBV-encoded latent membrane protein 1 (LMP1), which is commonly expressed in NPC, engages multiple signaling pathways that promote cell growth, transformation, and metabolic reprogramming. Here, we report a novel function of LMP1 in promoting de novo lipogenesis. LMP1 increases the expression, maturation and activation of sterol regulatory element-binding protein 1 (SREBP1), a master regulator of lipogenesis, and its downstream target fatty acid synthase (FASN). LMP1 also induces de novo lipid synthesis and lipid droplet formation. In contrast, small interfering RNA (siRNA) knockdown of LMP1 in EBV-infected epithelial cells diminished SREBP1 activation and lipid biosynthesis. Furthermore, inhibition of the mammalian target of rapamycin (mTOR) pathway, through the use of either mTOR inhibitors or siRNAs, significantly reduced LMP1-mediated SREBP1 activity and lipogenesis, indicating that LMP1 activation of the mTOR pathway is required for SREBP1-mediated lipogenesis. In primary NPC tumors, FASN overexpression is common, with high levels correlating significantly with LMP1 expression. Moreover, elevated FASN expression was associated with aggressive disease and poor survival in NPC patients. Luteolin and fatostatin, two inhibitors of lipogenesis, suppressed lipogenesis and proliferation of nasopharyngeal epithelial cells, effects that were more profound in cells expressing LMP1. Luteolin and fatostatin also dramatically inhibited NPC tumor growth in vitro and in vivo. Our findings demonstrate that LMP1 activation of SREBP1-mediated lipogenesis promotes tumor cell growth and is involved in EBV-driven NPC pathogenesis. Our results also reveal the therapeutic potential of utilizing lipogenesis inhibitors in the treatment of locally advanced or metastatic NPC. © 2018 The Authors. The Journal of Pathology published by John Wiley & Sons Ltd on behalf of Pathological Society of Great Britain and Ireland.</AbstractText>
<CopyrightInformation>© 2018 The Authors. The Journal of Pathology published by John Wiley & Sons Ltd on behalf of Pathological Society of Great Britain and Ireland.</CopyrightInformation>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Lo</LastName>
<ForeName>Angela Kwok-Fung</ForeName>
<Initials>AK</Initials>
<AffiliationInfo><Affiliation>Department of Anatomical and Cellular Pathology, Li Ka Shing Institute of Health Science, Chinese University of Hong Kong, Prince of Wales Hospital, Shatin, Hong Kong.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Lung</LastName>
<ForeName>Raymond Wai-Ming</ForeName>
<Initials>RW</Initials>
<AffiliationInfo><Affiliation>Department of Anatomical and Cellular Pathology, Li Ka Shing Institute of Health Science, Chinese University of Hong Kong, Prince of Wales Hospital, Shatin, Hong Kong.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Dawson</LastName>
<ForeName>Christopher W</ForeName>
<Initials>CW</Initials>
<AffiliationInfo><Affiliation>Institute of Cancer & Genomic Science, Cancer Research UK Cancer Centre, University of Birmingham, Birmingham, UK.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Young</LastName>
<ForeName>Lawrence S</ForeName>
<Initials>LS</Initials>
<AffiliationInfo><Affiliation>Warwick Medical School, University of Warwick, Coventry, UK.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Ko</LastName>
<ForeName>Chuen-Wai</ForeName>
<Initials>CW</Initials>
<AffiliationInfo><Affiliation>Department of Anatomical and Cellular Pathology, Li Ka Shing Institute of Health Science, Chinese University of Hong Kong, Prince of Wales Hospital, Shatin, Hong Kong.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Yeung</LastName>
<ForeName>Walter Wai</ForeName>
<Initials>WW</Initials>
<AffiliationInfo><Affiliation>Department of Anatomical and Cellular Pathology, Li Ka Shing Institute of Health Science, Chinese University of Hong Kong, Prince of Wales Hospital, Shatin, Hong Kong.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Kang</LastName>
<ForeName>Wei</ForeName>
<Initials>W</Initials>
<Identifier Source="ORCID">0000-0002-4651-677X</Identifier>
<AffiliationInfo><Affiliation>Department of Anatomical and Cellular Pathology, Li Ka Shing Institute of Health Science, Chinese University of Hong Kong, Prince of Wales Hospital, Shatin, Hong Kong.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>To</LastName>
<ForeName>Ka-Fai</ForeName>
<Initials>KF</Initials>
<AffiliationInfo><Affiliation>Department of Anatomical and Cellular Pathology, Li Ka Shing Institute of Health Science, Chinese University of Hong Kong, Prince of Wales Hospital, Shatin, Hong Kong.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Lo</LastName>
<ForeName>Kwok-Wai</ForeName>
<Initials>KW</Initials>
<Identifier Source="ORCID">0000-0002-3488-6124</Identifier>
<AffiliationInfo><Affiliation>Department of Anatomical and Cellular Pathology, Li Ka Shing Institute of Health Science, Chinese University of Hong Kong, Prince of Wales Hospital, Shatin, Hong Kong.</Affiliation>
</AffiliationInfo>
</Author>
</AuthorList>
<Language>eng</Language>
<PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType>
<PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType>
</PublicationTypeList>
<ArticleDate DateType="Electronic"><Year>2018</Year>
<Month>08</Month>
<Day>22</Day>
</ArticleDate>
</Article>
<MedlineJournalInfo><Country>England</Country>
<MedlineTA>J Pathol</MedlineTA>
<NlmUniqueID>0204634</NlmUniqueID>
<ISSNLinking>0022-3417</ISSNLinking>
</MedlineJournalInfo>
<ChemicalList><Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="C553294">1-(4-(4-propionylpiperazin-1-yl)-3-(trifluoromethyl)phenyl)-9-(quinolin-3-yl)benzo(h)(1,6)naphthyridin-2(1H)-one</NameOfSubstance>
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<NameOfSubstance UI="C558529">9-(6-aminopyridin-3-yl)-1-(3-(trifluoromethyl)phenyl)benzo(h)(1,6)naphthyridin-2(1H)-one</NameOfSubstance>
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<Chemical><RegistryNumber>0</RegistryNumber>
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<NameOfSubstance UI="C545733">fatostatin</NameOfSubstance>
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<MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000970" MajorTopicYN="N">Antineoplastic Agents</DescriptorName>
<QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D045744" MajorTopicYN="N">Cell Line, Tumor</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D049109" MajorTopicYN="Y">Cell Proliferation</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D018450" MajorTopicYN="N">Disease Progression</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D054890" MajorTopicYN="N">Fatty Acid Synthase, Type I</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D004854" MajorTopicYN="N">Herpesvirus 4, Human</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D066292" MajorTopicYN="N">Lipid Droplets</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D050155" MajorTopicYN="Y">Lipogenesis</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D047311" MajorTopicYN="N">Luteolin</DescriptorName>
<QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008807" MajorTopicYN="N">Mice, Inbred BALB C</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008819" MajorTopicYN="N">Mice, Nude</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName>
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<MeshHeading><DescriptorName UI="D009287" MajorTopicYN="N">Naphthyridines</DescriptorName>
<QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000077274" MajorTopicYN="N">Nasopharyngeal Carcinoma</DescriptorName>
<QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
<QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName>
<QualifierName UI="Q000821" MajorTopicYN="N">virology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D009303" MajorTopicYN="N">Nasopharyngeal Neoplasms</DescriptorName>
<QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
<QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName>
<QualifierName UI="Q000821" MajorTopicYN="N">virology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D011725" MajorTopicYN="N">Pyridines</DescriptorName>
<QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D051780" MajorTopicYN="N">Sterol Regulatory Element Binding Protein 1</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D058570" MajorTopicYN="N">TOR Serine-Threonine Kinases</DescriptorName>
<QualifierName UI="Q000037" MajorTopicYN="N">antagonists & inhibitors</QualifierName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D013844" MajorTopicYN="N">Thiazoles</DescriptorName>
<QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName>
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<MeshHeading><DescriptorName UI="D014763" MajorTopicYN="N">Viral Matrix Proteins</DescriptorName>
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<MeshHeading><DescriptorName UI="D023041" MajorTopicYN="N">Xenograft Model Antitumor Assays</DescriptorName>
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<Keyword MajorTopicYN="Y">LMP1</Keyword>
<Keyword MajorTopicYN="Y">SREBP1</Keyword>
<Keyword MajorTopicYN="Y">lipogenesis</Keyword>
<Keyword MajorTopicYN="Y">nasopharyngeal carcinoma</Keyword>
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   |texte=   Activation of sterol regulatory element-binding protein 1 (SREBP1)-mediated lipogenesis by the Epstein-Barr virus-encoded latent membrane protein 1 (LMP1) promotes cell proliferation and progression of nasopharyngeal carcinoma.
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Activation of sterol regulatory element-binding protein 1 (SREBP1)-mediated lipogenesis by the Epstein-Barr virus-encoded latent membrane protein 1 (LMP1) promotes cell proliferation and progression of nasopharyngeal carcinoma.

Activation of sterol regulatory element-binding protein 1 (SREBP1)-mediated lipogenesis by the Epstein-Barr virus-encoded latent membrane protein 1 (LMP1) promotes cell proliferation and progression of nasopharyngeal carcinoma.

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