Human Papillomavirus 11 Early Protein E6 Activates Autophagy by Repressing AKT/mTOR and Erk/mTOR
Identifieur interne : 000368 ( Pmc/Curation ); précédent : 000367; suivant : 000369Human Papillomavirus 11 Early Protein E6 Activates Autophagy by Repressing AKT/mTOR and Erk/mTOR
Auteurs : Boya Zhang [République populaire de Chine] ; Yinjing Song [République populaire de Chine] ; Siyuan Sun [République populaire de Chine] ; Rui Han [République populaire de Chine] ; Chunting Hua [République populaire de Chine] ; Stijn Van Der Veen [République populaire de Chine] ; Hao Cheng [République populaire de Chine]Source :
- Journal of Virology [ 0022-538X ] ; 2019.
Abstract
We transfected an HPV11 E6 plasmid into HaCaT cells, H8 cells, and NHEK cells and established a stable cell line expressing the HPV11 E6 protein. Then, we confirmed that HPV11 E6 induces autophagy by suppressing the AKT/mTOR and Erk/mTOR pathways. In contrast to the high-risk HPV E6 genes, HPV11 E6 did not affect the expression of p53. To the best of our knowledge, this study represents the first direct in-depth investigation of the relationship between the LR-HPV E6 gene and autophagy, which may help to reveal the pathogenesis of LR-HPV infection.
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DOI: 10.1128/JVI.00172-19
PubMed: 30971468
PubMed Central: 6613752
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China</addr-line></nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Dermatology, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou</wicri:regionArea></affiliation></author><author><name sortKey="Sun, Siyuan" sort="Sun, Siyuan" uniqKey="Sun S" first="Siyuan" last="Sun">Siyuan Sun</name><affiliation wicri:level="1"><nlm:aff id="aff1"><addr-line>Department of Dermatology, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, China</addr-line></nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Dermatology, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou</wicri:regionArea></affiliation></author><author><name sortKey="Han, Rui" sort="Han, Rui" uniqKey="Han R" first="Rui" last="Han">Rui Han</name><affiliation wicri:level="1"><nlm:aff id="aff1"><addr-line>Department of Dermatology, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, China</addr-line></nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Dermatology, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou</wicri:regionArea></affiliation></author><author><name sortKey="Hua, Chunting" sort="Hua, Chunting" uniqKey="Hua C" first="Chunting" last="Hua">Chunting Hua</name><affiliation wicri:level="1"><nlm:aff id="aff1"><addr-line>Department of Dermatology, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, China</addr-line></nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Dermatology, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou</wicri:regionArea></affiliation></author><author><name sortKey="Van Der Veen, Stijn" sort="Van Der Veen, Stijn" uniqKey="Van Der Veen S" first="Stijn" last="Van Der Veen">Stijn Van Der 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sortKey="Cheng, Hao" sort="Cheng, Hao" uniqKey="Cheng H" first="Hao" last="Cheng">Hao Cheng</name><affiliation wicri:level="1"><nlm:aff id="aff1"><addr-line>Department of Dermatology, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, China</addr-line></nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Dermatology, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou</wicri:regionArea></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">30971468</idno><idno type="pmc">6613752</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6613752</idno><idno type="RBID">PMC:6613752</idno><idno type="doi">10.1128/JVI.00172-19</idno><date when="2019">2019</date><idno type="wicri:Area/Pmc/Corpus">000368</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000368</idno><idno 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wicri:level="1"><nlm:aff id="aff1"><addr-line>Department of Dermatology, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, China</addr-line></nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Dermatology, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou</wicri:regionArea></affiliation></author><author><name sortKey="Sun, Siyuan" sort="Sun, Siyuan" uniqKey="Sun S" first="Siyuan" last="Sun">Siyuan Sun</name><affiliation wicri:level="1"><nlm:aff id="aff1"><addr-line>Department of Dermatology, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, China</addr-line></nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Dermatology, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou</wicri:regionArea></affiliation></author><author><name sortKey="Han, Rui" sort="Han, Rui" uniqKey="Han R" first="Rui" last="Han">Rui Han</name><affiliation wicri:level="1"><nlm:aff id="aff1"><addr-line>Department of Dermatology, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, China</addr-line></nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Dermatology, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou</wicri:regionArea></affiliation></author><author><name sortKey="Hua, Chunting" sort="Hua, Chunting" uniqKey="Hua C" first="Chunting" last="Hua">Chunting Hua</name><affiliation wicri:level="1"><nlm:aff id="aff1"><addr-line>Department of Dermatology, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, China</addr-line></nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Dermatology, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou</wicri:regionArea></affiliation></author><author><name sortKey="Van Der Veen, Stijn" sort="Van Der Veen, Stijn" uniqKey="Van Der Veen S" first="Stijn" last="Van Der Veen">Stijn Van Der Veen</name><affiliation wicri:level="1"><nlm:aff id="aff1"><addr-line>Department of Dermatology, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, China</addr-line></nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Dermatology, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="aff2"><addr-line>Department of Microbiology and Parasitology, Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, School of Medicine, Zhejiang University, Hangzhou, China</addr-line></nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Microbiology and Parasitology, Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, School of Medicine, Zhejiang University, Hangzhou</wicri:regionArea></affiliation></author><author><name sortKey="Cheng, Hao" sort="Cheng, Hao" uniqKey="Cheng H" first="Hao" last="Cheng">Hao Cheng</name><affiliation wicri:level="1"><nlm:aff id="aff1"><addr-line>Department of Dermatology, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, China</addr-line></nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Dermatology, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou</wicri:regionArea></affiliation></author></analytic><series><title level="j">Journal of Virology</title><idno type="ISSN">0022-538X</idno><idno type="eISSN">1098-5514</idno><imprint><date when="2019">2019</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>We transfected an HPV11 E6 plasmid into HaCaT cells, H8 cells, and NHEK cells and established a stable cell line expressing the HPV11 E6 protein. Then, we confirmed that HPV11 E6 induces autophagy by suppressing the AKT/mTOR and Erk/mTOR pathways. In contrast to the high-risk HPV E6 genes, HPV11 E6 did not affect the expression of p53. To the best of our knowledge, this study represents the first direct in-depth investigation of the relationship between the LR-HPV E6 gene and autophagy, which may help to reveal the pathogenesis of LR-HPV infection.</p></div></front></TEI><pmc article-type="research-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<front><journal-meta><journal-id journal-id-type="nlm-ta">J Virol</journal-id><journal-id journal-id-type="iso-abbrev">J. Virol</journal-id><journal-id journal-id-type="hwp">jvi</journal-id><journal-id journal-id-type="pmc">jvi</journal-id><journal-id journal-id-type="publisher-id">JVI</journal-id><journal-title-group><journal-title>Journal of Virology</journal-title></journal-title-group><issn pub-type="ppub">0022-538X</issn><issn pub-type="epub">1098-5514</issn><publisher><publisher-name>American Society for Microbiology</publisher-name><publisher-loc>1752 N St., N.W., Washington, DC</publisher-loc></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">30971468</article-id><article-id pub-id-type="pmc">6613752</article-id><article-id pub-id-type="publisher-id">00172-19</article-id><article-id pub-id-type="doi">10.1128/JVI.00172-19</article-id><article-categories><subj-group subj-group-type="heading"><subject>Virus-Cell Interactions</subject></subj-group></article-categories><title-group><article-title>Human Papillomavirus 11 Early Protein E6 Activates Autophagy by Repressing AKT/mTOR and Erk/mTOR</article-title><alt-title alt-title-type="running-head">HPV 11E6 Induces Autophagy by mTOR Pathway</alt-title><alt-title alt-title-type="short-authors">Zhang et al.</alt-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Zhang</surname><given-names>Boya</given-names></name><xref ref-type="aff" rid="aff1"><sup>a</sup></xref></contrib><contrib contrib-type="author"><name><surname>Song</surname><given-names>Yinjing</given-names></name><xref ref-type="aff" rid="aff1"><sup>a</sup></xref></contrib><contrib contrib-type="author"><name><surname>Sun</surname><given-names>Siyuan</given-names></name><xref ref-type="aff" rid="aff1"><sup>a</sup></xref></contrib><contrib contrib-type="author"><name><surname>Han</surname><given-names>Rui</given-names></name><xref ref-type="aff" rid="aff1"><sup>a</sup></xref></contrib><contrib contrib-type="author"><name><surname>Hua</surname><given-names>Chunting</given-names></name><xref ref-type="aff" rid="aff1"><sup>a</sup></xref></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid" authenticated="false">https://orcid.org/0000-0002-8176-391X</contrib-id><name><surname>van der Veen</surname><given-names>Stijn</given-names></name><xref ref-type="aff" rid="aff1"><sup>a</sup></xref><xref ref-type="aff" rid="aff2"><sup>b</sup></xref></contrib><contrib contrib-type="author" corresp="yes"><name><surname>Cheng</surname><given-names>Hao</given-names></name><xref ref-type="aff" rid="aff1"><sup>a</sup></xref></contrib><aff id="aff1"><label>a</label><addr-line>Department of Dermatology, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, China</addr-line></aff><aff id="aff2"><label>b</label><addr-line>Department of Microbiology and Parasitology, Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, School of Medicine, Zhejiang University, Hangzhou, China</addr-line></aff></contrib-group><contrib-group><contrib contrib-type="editor"><name><surname>Banks</surname><given-names>Lawrence</given-names></name><role>Editor</role><aff>International Centre for Genetic Engineering and Biotechnology</aff></contrib></contrib-group><author-notes><corresp id="cor1">Address correspondence to Stijn van der Veen, <email>stijnvanderveen@zju.edu.cn</email>, or Hao Cheng, <email>chenghao1@zju.edu.cn</email>.</corresp><fn fn-type="other"><p><bold>Citation</bold> Zhang B, Song Y, Sun S, Han R, Hua C, van der Veen S, Cheng H. 2019. Human papillomavirus 11 early protein E6 activates autophagy by repressing AKT/mTOR and Erk/mTOR. J Virol 93:e00172-19. <ext-link ext-link-type="uri" xlink:href="https://doi.org/10.1128/JVI.00172-19">https://doi.org/10.1128/JVI.00172-19</ext-link>.</p></fn></author-notes><pub-date pub-type="epreprint"><day>10</day><month>4</month><year>2019</year></pub-date><pub-date pub-type="epub"><day>29</day><month>5</month><year>2019</year></pub-date><pub-date pub-type="collection"><day>15</day><month>6</month><year>2019</year></pub-date><volume>93</volume><issue>12</issue><elocation-id>e00172-19</elocation-id><history><date date-type="received"><day>4</day><month>2</month><year>2019</year></date><date date-type="accepted"><day>31</day><month>3</month><year>2019</year></date></history><permissions><copyright-statement>Copyright © 2019 American Society for Microbiology.</copyright-statement><copyright-year>2019</copyright-year><copyright-holder>American Society for Microbiology</copyright-holder><license license-type="asm" xlink:href="https://doi.org/10.1128/ASMCopyrightv2"><license-p><ext-link ext-link-type="uri" xlink:href="https://doi.org/10.1128/ASMCopyrightv2">All Rights Reserved</ext-link>.</license-p></license></permissions><self-uri content-type="pdf" xlink:href="JVI.00172-19.pdf"></self-uri><abstract abstract-type="precis"><p>We transfected an HPV11 E6 plasmid into HaCaT cells, H8 cells, and NHEK cells and established a stable cell line expressing the HPV11 E6 protein. Then, we confirmed that HPV11 E6 induces autophagy by suppressing the AKT/mTOR and Erk/mTOR pathways. In contrast to the high-risk HPV E6 genes, HPV11 E6 did not affect the expression of p53. To the best of our knowledge, this study represents the first direct in-depth investigation of the relationship between the LR-HPV E6 gene and autophagy, which may help to reveal the pathogenesis of LR-HPV infection.</p></abstract><abstract><title>ABSTRACT</title><p>Low-risk human papillomaviruses (LR-HPVs) are the causative agents of genital warts, which are a widespread sexually transmitted disease. How LR-HPVs affect autophagy and the specific proteins involved are unknown. In the current study, we investigated the impact of LR-HPV11 early protein 6 (E6) on the activity of the autophagy pathway. We transfected an HPV11 E6 (11E6) plasmid into HaCaT cells, H8 cells, and NHEK cells and established a stable cell line expressing the HPV11 E6 protein. The differences in autophagy activity and upstream regulatory pathways compared with those in the parent cell lines were investigated using a Western blot analysis of the total and phosphorylated protein levels and confocal microscopy of immunostained cells and cells transfected with an mCherry-green fluorescent protein-LC3 expression plasmid. We used short hairpin RNA (shRNA) to knock down 11E6 and showed that these effects require continued 11E6 expression. Compared with its expression in the control cells, the expression of HPV11 E6 in the cells activated the autophagy pathway. The increased autophagy activity was the result of the decreased phosphorylation levels of the canonical autophagy repressor mammalian target of rapamycin (mTOR) at its Ser2448 position (the mTOR complex 1 [mTORC1] phosphorylation site) and decreased AKT and Erk phosphorylation. Therefore, these results indicate that HPV11 E6 activates autophagy through the AKT/mTOR and Erk/mTOR pathways. Our findings provide novel insight into the relationship between LR-HPV infections and autophagy and could help elucidate the pathogenic mechanisms of LR-HPV.</p><p><bold>IMPORTANCE</bold> We transfected an HPV11 E6 plasmid into HaCaT cells, H8 cells, and NHEK cells and established a stable cell line expressing the HPV11 E6 protein. Then, we confirmed that HPV11 E6 induces autophagy by suppressing the AKT/mTOR and Erk/mTOR pathways. In contrast to the high-risk HPV E6 genes, HPV11 E6 did not affect the expression of p53. To the best of our knowledge, this study represents the first direct in-depth investigation of the relationship between the LR-HPV E6 gene and autophagy, which may help to reveal the pathogenesis of LR-HPV infection.</p></abstract><kwd-group><title>KEYWORDS</title><kwd>AKT/mTOR</kwd><kwd>E6</kwd><kwd>Erk/mTOR</kwd><kwd>LR-HPV</kwd><kwd>autophagy</kwd></kwd-group><funding-group><award-group id="award1"><funding-source><institution-wrap><institution>National Natural Science Foundation of China (NSFC)</institution><institution-id>https://doi.org/10.13039/501100001809</institution-id></institution-wrap></funding-source><award-id>81573057</award-id><principal-award-recipient><name><surname>Zhang</surname><given-names>Boya</given-names></name></principal-award-recipient></award-group><award-group id="award2"><funding-source><institution-wrap><institution>National Natural Science Foundation of China (NSFC)</institution><institution-id>https://doi.org/10.13039/501100001809</institution-id></institution-wrap></funding-source><award-id>81472889</award-id><principal-award-recipient><name><surname>Cheng</surname><given-names>Hao</given-names></name></principal-award-recipient></award-group><award-group id="award3"><funding-source><institution-wrap><institution>National Health and Family Planning Commission of the People's Republic of China (Ministry of Health of China)</institution><institution-id>https://doi.org/10.13039/501100004572</institution-id></institution-wrap></funding-source><award-id>2015117502</award-id><principal-award-recipient><name><surname>Song</surname><given-names>Yinjing</given-names></name></principal-award-recipient></award-group><award-group id="award4"><funding-source><institution-wrap><institution>Science and Technology Department of Zhejiang Province</institution><institution-id>https://doi.org/10.13039/501100008990</institution-id></institution-wrap></funding-source><award-id>2018C04013</award-id><principal-award-recipient><name><surname>Sun</surname><given-names>Siyuan</given-names></name></principal-award-recipient></award-group></funding-group><counts><fig-count count="7"></fig-count><table-count count="2"></table-count><equation-count count="0"></equation-count><ref-count count="76"></ref-count><page-count count="16"></page-count><word-count count="9614"></word-count></counts><custom-meta-group><custom-meta><meta-name>cover-date</meta-name><meta-value>June 2019</meta-value></custom-meta></custom-meta-group></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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