LMP1 signaling pathway activates IRF4 in latent EBV infection and a positive circuit between PI3K and Src is required
Interferon (IFN) regulatory factors (IRFs) have crucial roles in immune regulation and oncogenesis. We have recently shown that IRF4 is activated through c-Src-mediated tyrosine phosphorylation in virus-transformed cells. However, the intracellular signaling pathway triggering Src activation of IRF4...
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| Veröffentlicht in: | Oncogene 2017-04, Vol.36 (16), p.2265-2274 |
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| creator | Wang, L Ren, J Li, G Moorman, J P Yao, Z Q Ning, S |
| description | Interferon (IFN) regulatory factors (IRFs) have crucial roles in immune regulation and oncogenesis. We have recently shown that IRF4 is activated through c-Src-mediated tyrosine phosphorylation in virus-transformed cells. However, the intracellular signaling pathway triggering Src activation of IRF4 remains unknown. In this study, we provide evidence that Epstein–Barr virus (EBV) latent membrane protein 1 (LMP1) promotes IRF4 phosphorylation and markedly stimulates IRF4 transcriptional activity, and that Src mediates LMP1 activation of IRF4. As to more precise mechanism, we show that LMP1 physically interacts with c-Src, and the phosphatidylinositol 3 kinase (PI3K) subunit P85 mediates their interaction. Depletion of P85 by P85-specific short hairpin RNAs disrupts their interaction and diminishes IRF4 phosphorylation in EBV-transformed cells. Furthermore, we show that Src is upstream of PI3K for activation of both IRF4 and Akt. In turn, inhibition of PI3K kinase activity by the PI3K-speicfic inhibitor LY294002 impairs Src activity. Our results show that LMP1 signaling is responsible for IRF4 activation, and further characterize the IRF4 regulatory network that is a promising therapeutic target for specific hematological malignancies. |
| doi_str_mv | 10.1038/onc.2016.380 |
| format | Article |
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We have recently shown that IRF4 is activated through c-Src-mediated tyrosine phosphorylation in virus-transformed cells. However, the intracellular signaling pathway triggering Src activation of IRF4 remains unknown. In this study, we provide evidence that Epstein–Barr virus (EBV) latent membrane protein 1 (LMP1) promotes IRF4 phosphorylation and markedly stimulates IRF4 transcriptional activity, and that Src mediates LMP1 activation of IRF4. As to more precise mechanism, we show that LMP1 physically interacts with c-Src, and the phosphatidylinositol 3 kinase (PI3K) subunit P85 mediates their interaction. Depletion of P85 by P85-specific short hairpin RNAs disrupts their interaction and diminishes IRF4 phosphorylation in EBV-transformed cells. Furthermore, we show that Src is upstream of PI3K for activation of both IRF4 and Akt. In turn, inhibition of PI3K kinase activity by the PI3K-speicfic inhibitor LY294002 impairs Src activity. Our results show that LMP1 signaling is responsible for IRF4 activation, and further characterize the IRF4 regulatory network that is a promising therapeutic target for specific hematological malignancies.</description><identifier>ISSN: 0950-9232</identifier><identifier>EISSN: 1476-5594</identifier><identifier>DOI: 10.1038/onc.2016.380</identifier><identifier>PMID: 27819673</identifier><identifier>CODEN: ONCNES</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>1-Phosphatidylinositol 3-kinase ; 38/77 ; 45/15 ; 631/326/596 ; 692/53 ; 96/109 ; 96/31 ; AKT protein ; Apoptosis ; Carcinogenesis ; Cell Biology ; Cell Line ; Cellular signal transduction ; Class Ia Phosphatidylinositol 3-Kinase - metabolism ; Epstein-Barr virus ; Epstein-Barr Virus Infections - metabolism ; Gene expression ; Genetic aspects ; Health aspects ; HEK293 Cells ; Human Genetics ; Humans ; Immunoregulation ; Infections ; Interferon ; Interferon regulatory factor 4 ; Interferon Regulatory Factors - genetics ; Interferon Regulatory Factors - metabolism ; Internal Medicine ; Intracellular signalling ; Kinases ; Latent membrane protein 1 ; Medicine ; Medicine & Public Health ; Membrane proteins ; Neurons ; Oncology ; original-article ; Phosphorylation ; Proto-Oncogene Proteins pp60(c-src) - antagonists & inhibitors ; Proto-Oncogene Proteins pp60(c-src) - metabolism ; Signal Transduction ; Signaling ; Src protein ; Therapeutic targets ; Transcription ; Transcription factors ; Transcriptional Activation ; Transformed cells ; Tumorigenesis ; Tyrosine ; Viral Matrix Proteins - metabolism ; Viral proteins</subject><ispartof>Oncogene, 2017-04, Vol.36 (16), p.2265-2274</ispartof><rights>Macmillan Publishers Limited, part of Springer Nature. 2017</rights><rights>COPYRIGHT 2017 Nature Publishing Group</rights><rights>Copyright Nature Publishing Group Apr 20, 2017</rights><rights>Macmillan Publishers Limited, part of Springer Nature. 2017.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c605t-f4f40dd4c397ec7e5712ee3f9aa6494b7be738b00908605feb26bbcc7e8655963</citedby><cites>FETCH-LOGICAL-c605t-f4f40dd4c397ec7e5712ee3f9aa6494b7be738b00908605feb26bbcc7e8655963</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1038/onc.2016.380$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/onc.2016.380$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>230,314,776,780,881,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27819673$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wang, L</creatorcontrib><creatorcontrib>Ren, J</creatorcontrib><creatorcontrib>Li, G</creatorcontrib><creatorcontrib>Moorman, J P</creatorcontrib><creatorcontrib>Yao, Z Q</creatorcontrib><creatorcontrib>Ning, S</creatorcontrib><title>LMP1 signaling pathway activates IRF4 in latent EBV infection and a positive circuit between PI3K and Src is required</title><title>Oncogene</title><addtitle>Oncogene</addtitle><addtitle>Oncogene</addtitle><description>Interferon (IFN) regulatory factors (IRFs) have crucial roles in immune regulation and oncogenesis. We have recently shown that IRF4 is activated through c-Src-mediated tyrosine phosphorylation in virus-transformed cells. However, the intracellular signaling pathway triggering Src activation of IRF4 remains unknown. In this study, we provide evidence that Epstein–Barr virus (EBV) latent membrane protein 1 (LMP1) promotes IRF4 phosphorylation and markedly stimulates IRF4 transcriptional activity, and that Src mediates LMP1 activation of IRF4. As to more precise mechanism, we show that LMP1 physically interacts with c-Src, and the phosphatidylinositol 3 kinase (PI3K) subunit P85 mediates their interaction. Depletion of P85 by P85-specific short hairpin RNAs disrupts their interaction and diminishes IRF4 phosphorylation in EBV-transformed cells. Furthermore, we show that Src is upstream of PI3K for activation of both IRF4 and Akt. In turn, inhibition of PI3K kinase activity by the PI3K-speicfic inhibitor LY294002 impairs Src activity. Our results show that LMP1 signaling is responsible for IRF4 activation, and further characterize the IRF4 regulatory network that is a promising therapeutic target for specific hematological malignancies.</description><subject>1-Phosphatidylinositol 3-kinase</subject><subject>38/77</subject><subject>45/15</subject><subject>631/326/596</subject><subject>692/53</subject><subject>96/109</subject><subject>96/31</subject><subject>AKT protein</subject><subject>Apoptosis</subject><subject>Carcinogenesis</subject><subject>Cell Biology</subject><subject>Cell Line</subject><subject>Cellular signal transduction</subject><subject>Class Ia Phosphatidylinositol 3-Kinase - metabolism</subject><subject>Epstein-Barr virus</subject><subject>Epstein-Barr Virus Infections - metabolism</subject><subject>Gene expression</subject><subject>Genetic aspects</subject><subject>Health aspects</subject><subject>HEK293 Cells</subject><subject>Human Genetics</subject><subject>Humans</subject><subject>Immunoregulation</subject><subject>Infections</subject><subject>Interferon</subject><subject>Interferon regulatory factor 4</subject><subject>Interferon Regulatory Factors - 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metabolism</topic><topic>Viral proteins</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wang, L</creatorcontrib><creatorcontrib>Ren, J</creatorcontrib><creatorcontrib>Li, G</creatorcontrib><creatorcontrib>Moorman, J P</creatorcontrib><creatorcontrib>Yao, Z Q</creatorcontrib><creatorcontrib>Ning, S</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Biological Science Database</collection><collection>Research Library (Corporate)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest Central (New)</collection><collection>ProQuest One Academic (New)</collection><collection>ProQuest Health & Medical Research Collection</collection><collection>ProQuest One Academic Middle East (New)</collection><collection>ProQuest One Health & Nursing</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Applied & Life Sciences</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Oncogene</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wang, L</au><au>Ren, J</au><au>Li, G</au><au>Moorman, J P</au><au>Yao, Z Q</au><au>Ning, S</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>LMP1 signaling pathway activates IRF4 in latent EBV infection and a positive circuit between PI3K and Src is required</atitle><jtitle>Oncogene</jtitle><stitle>Oncogene</stitle><addtitle>Oncogene</addtitle><date>2017-04-20</date><risdate>2017</risdate><volume>36</volume><issue>16</issue><spage>2265</spage><epage>2274</epage><pages>2265-2274</pages><issn>0950-9232</issn><eissn>1476-5594</eissn><coden>ONCNES</coden><abstract>Interferon (IFN) regulatory factors (IRFs) have crucial roles in immune regulation and oncogenesis. We have recently shown that IRF4 is activated through c-Src-mediated tyrosine phosphorylation in virus-transformed cells. However, the intracellular signaling pathway triggering Src activation of IRF4 remains unknown. In this study, we provide evidence that Epstein–Barr virus (EBV) latent membrane protein 1 (LMP1) promotes IRF4 phosphorylation and markedly stimulates IRF4 transcriptional activity, and that Src mediates LMP1 activation of IRF4. As to more precise mechanism, we show that LMP1 physically interacts with c-Src, and the phosphatidylinositol 3 kinase (PI3K) subunit P85 mediates their interaction. Depletion of P85 by P85-specific short hairpin RNAs disrupts their interaction and diminishes IRF4 phosphorylation in EBV-transformed cells. Furthermore, we show that Src is upstream of PI3K for activation of both IRF4 and Akt. In turn, inhibition of PI3K kinase activity by the PI3K-speicfic inhibitor LY294002 impairs Src activity. Our results show that LMP1 signaling is responsible for IRF4 activation, and further characterize the IRF4 regulatory network that is a promising therapeutic target for specific hematological malignancies.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>27819673</pmid><doi>10.1038/onc.2016.380</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | 1-Phosphatidylinositol 3-kinase 38/77 45/15 631/326/596 692/53 96/109 96/31 AKT protein Apoptosis Carcinogenesis Cell Biology Cell Line Cellular signal transduction Class Ia Phosphatidylinositol 3-Kinase - metabolism Epstein-Barr virus Epstein-Barr Virus Infections - metabolism Gene expression Genetic aspects Health aspects HEK293 Cells Human Genetics Humans Immunoregulation Infections Interferon Interferon regulatory factor 4 Interferon Regulatory Factors - genetics Interferon Regulatory Factors - metabolism Internal Medicine Intracellular signalling Kinases Latent membrane protein 1 Medicine Medicine & Public Health Membrane proteins Neurons Oncology original-article Phosphorylation Proto-Oncogene Proteins pp60(c-src) - antagonists & inhibitors Proto-Oncogene Proteins pp60(c-src) - metabolism Signal Transduction Signaling Src protein Therapeutic targets Transcription Transcription factors Transcriptional Activation Transformed cells Tumorigenesis Tyrosine Viral Matrix Proteins - metabolism Viral proteins |
| title | LMP1 signaling pathway activates IRF4 in latent EBV infection and a positive circuit between PI3K and Src is required |
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