Cyclooxygenase-2-prostaglandin E2-eicosanoid receptor inflammatory axis: a key player in Kaposi's sarcoma-associated herpes virus associated malignancies
2013; Elsevier BV; Volume: 162; Issue: 2 Linguagem: Inglês
10.1016/j.trsl.2013.03.004
ISSN1931-5244
AutoresArun George Paul, Bala Chandran, Neelam Sharma-Walia,
Tópico(s)Inflammatory mediators and NSAID effects
ResumoThe role of cyclooxygenase-2 (COX-2), its lipid metabolite prostaglandin E2 (PGE2), and Eicosanoid (EP) receptors (EP; 1-4) underlying the proinflammatory mechanistic aspects of Burkitt's lymphoma, nasopharyngeal carcinoma, cervical cancer, prostate cancer, colon cancer, and Kaposi's sarcoma (KS) is an active area of investigation. The tumorigenic potential of COX-2 and PGE2 through EP receptors forms the mechanistic context underlying the chemotherapeutic potential of nonsteroidal anti-inflammatory drugs (NSAIDs). Although role of the COX-2 is described in several viral associated malignancies, the biological significance of the COX-2/PGE2/EP receptor inflammatory axis is extensively studied only in Kaposi's sarcoma-associated herpes virus (KSHV/HHV-8) associated malignancies such as KS, a multifocal endothelial cell tumor and primary effusion lymphoma (PEL), a B cell-proliferative disorder. The purpose of this review is to summarize the salient findings delineating the molecular mechanisms downstream of COX-2 involving PGE2 secretion and its autocrine and paracrine interactions with EP receptors (EP1-4), COX-2/PGE2/EP receptor signaling regulating KSHV pathogenesis and latency. KSHV infection induces COX-2, PGE2 secretion, and EP receptor activation. The resulting signal cascades modulate the expression of KSHV latency genes (latency associated nuclear antigen-1 [LANA-1] and viral-Fas (TNFRSF6)-associated via death domain like interferon converting enzyme-like- inhibitory protein [vFLIP]). vFLIP was also shown to be crucial for the maintenance of COX-2 activation. The mutually interdependent interactions between viral proteins (LANA-1/vFLIP) and COX-2/PGE2/EP receptors was shown to play key roles in the biological mechanisms involved in KS and PEL pathogenesis such as blockage of apoptosis, cell cycle regulation, transformation, proliferation, angiogenesis, adhesion, invasion, and immune-suppression. Understanding the COX-2/PGE2/EP axis is very important to develop new safer and specific therapeutic modalities for KS and PEL. In addition to COX-2 being a therapeutic target, EP receptors represent ideal targets for pharmacologic agents as PGE2 analogues and their blockers/antagonists possess antineoplastic activity, without the reported gastrointestinal and cardiovascular toxicity observed with few a NSAIDs. The role of cyclooxygenase-2 (COX-2), its lipid metabolite prostaglandin E2 (PGE2), and Eicosanoid (EP) receptors (EP; 1-4) underlying the proinflammatory mechanistic aspects of Burkitt's lymphoma, nasopharyngeal carcinoma, cervical cancer, prostate cancer, colon cancer, and Kaposi's sarcoma (KS) is an active area of investigation. The tumorigenic potential of COX-2 and PGE2 through EP receptors forms the mechanistic context underlying the chemotherapeutic potential of nonsteroidal anti-inflammatory drugs (NSAIDs). Although role of the COX-2 is described in several viral associated malignancies, the biological significance of the COX-2/PGE2/EP receptor inflammatory axis is extensively studied only in Kaposi's sarcoma-associated herpes virus (KSHV/HHV-8) associated malignancies such as KS, a multifocal endothelial cell tumor and primary effusion lymphoma (PEL), a B cell-proliferative disorder. The purpose of this review is to summarize the salient findings delineating the molecular mechanisms downstream of COX-2 involving PGE2 secretion and its autocrine and paracrine interactions with EP receptors (EP1-4), COX-2/PGE2/EP receptor signaling regulating KSHV pathogenesis and latency. KSHV infection induces COX-2, PGE2 secretion, and EP receptor activation. The resulting signal cascades modulate the expression of KSHV latency genes (latency associated nuclear antigen-1 [LANA-1] and viral-Fas (TNFRSF6)-associated via death domain like interferon converting enzyme-like- inhibitory protein [vFLIP]). vFLIP was also shown to be crucial for the maintenance of COX-2 activation. The mutually interdependent interactions between viral proteins (LANA-1/vFLIP) and COX-2/PGE2/EP receptors was shown to play key roles in the biological mechanisms involved in KS and PEL pathogenesis such as blockage of apoptosis, cell cycle regulation, transformation, proliferation, angiogenesis, adhesion, invasion, and immune-suppression. Understanding the COX-2/PGE2/EP axis is very important to develop new safer and specific therapeutic modalities for KS and PEL. In addition to COX-2 being a therapeutic target, EP receptors represent ideal targets for pharmacologic agents as PGE2 analogues and their blockers/antagonists possess antineoplastic activity, without the reported gastrointestinal and cardiovascular toxicity observed with few a NSAIDs. In the 19th century, Rudolf Virchow first proposed a potential link between inflammation and cancer based on his observations on the presence of leukocytes in tumors.1Grivennikov S.I. Greten F.R. Karin M. Immunity, inflammation, and cancer.Cell. 2010; 140: 883-899Abstract Full Text Full Text PDF PubMed Google Scholar Inflammation is a physiological mechanism evolved for wound healing and therefore is counter-intuitive to consider it to be oncogenic. Nevertheless, inflammation is a 'double-edged sword' with a pathologic edge that can promote various aspects of tumorigenesis deregulated such as cell proliferation, migration, angiogenesis, and apoptosis.1Grivennikov S.I. Greten F.R. Karin M. Immunity, inflammation, and cancer.Cell. 2010; 140: 883-899Abstract Full Text Full Text PDF PubMed Google Scholar Within the last decade, a multitude of studies demonstrating the a) abundance of inflammatory cells such as macrophages and fibroblasts in cancer biopsies, b) the role of proinflammatory molecules such as cyclooxygenase-2 (COX-2), prostaglandin E2, leukotrienes, transforming growth factor beta (TGF-β), hypoxia inducible factor-1 alpha, vascular endothelial growth factor (VEGF), nitric oxide synthase, nitric oxide, reactive oxygen species (ROS), cytokines and chemokines in the pathogenesis of several cancers, and the tumorigenic nurturing properties of the proinflammatory tumor microenvironment strongly indicates that inflammation plays a pathogenic role in several cancers.1Grivennikov S.I. Greten F.R. Karin M. Immunity, inflammation, and cancer.Cell. 2010; 140: 883-899Abstract Full Text Full Text PDF PubMed Google Scholar, 2Rakoff-Nahoum S. 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Cancer-related inflammation.Nature. 2008; 454: 436-444Crossref PubMed Google Scholar Chronic persistent inflammation is believed to play an important role in the pathogenesis of 15% of all malignancies.1Grivennikov S.I. Greten F.R. Karin M. Immunity, inflammation, and cancer.Cell. 2010; 140: 883-899Abstract Full Text Full Text PDF PubMed Google Scholar, 2Rakoff-Nahoum S. Why cancer and inflammation?.Yale J Biol Med. 2006; 79: 123-130PubMed Google Scholar, 3Coussens L.M. Werb Z. Inflammation and cancer.Nature. 2002; 420: 860-867Crossref PubMed Google Scholar, 4Balkwill F. Mantovani A. Inflammation and cancer: back to Virchow?.Lancet. 2001; 357: 539-545Abstract Full Text Full Text PDF PubMed Google Scholar, 5Wang D. Dubois R.N. Prostaglandins and cancer.Gut. 2006; 55: 115-122Crossref PubMed Google Scholar Depending on the type and stage of cancer, the physiological to pathologic switch of inflammation is triggered by various factors such as genomic instability, epigenetic changes, somatic mutations, tumor suppressor and oncogene mediated carcinogenesis, chronic persistent infections, and environmental stressors such as pollutants.1Grivennikov S.I. Greten F.R. Karin M. Immunity, inflammation, and cancer.Cell. 2010; 140: 883-899Abstract Full Text Full Text PDF PubMed Google Scholar, 7Kundu J.K. Surh Y.J. Inflammation: gearing the journey to cancer.Mutat Res. 2008; 659: 15-30Crossref PubMed Google Scholar, 8Mantovani A. Allavena P. Sica A. Balkwill F. Cancer-related inflammation.Nature. 2008; 454: 436-444Crossref PubMed Google Scholar The role of tumor viruses in chronic persistent inflammation associated carcinogenesis is demonstrated in several malignancies such as Kaposi's sarcoma associated-herpes virus (KSHV/HHV-8) in Kaposi's sarcoma (KS) and primary effusion lymphoma (PEL), Epstein-Barr virus (EBV) in Burkitt's lymphoma and nasopharyngeal carcinoma, human papillomavirus (HPV) in cervical cancer, hepatitis B (HBV) and hepatitis C viruses (HCV) in hepatocellular cancer, and human T-lymphotropic virus (HTLV) in T-cell leukemia.6Sinkovics J.G. Molecular biology of oncogenic inflammatory processes. I. Nononcogenic and oncogenic pathogens, intrinsic inflammatory reactions without pathogens, and microRNA/DNA interactions (Review).Int J Oncol. 2012; 40: 305-349PubMed Google Scholar, 9Taylor G.S. Blackbourn D.J. 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Complement and infectious agents: a tale of disguise and deception.Complement Inflamm. 1989; 6: 249-258PubMed Google Scholar Piracy of inflammatory mechanisms is a recurring theme in the story of infections by KSHV, EBV, HCV, HPV, HBV, and HTLV because of the proliferative, angiogenic, immune-suppressive, and antiapoptotic niche that persistent inflammation provides.11Saha A. Kaul R. Murakami M. Robertson E.S. Tumor viruses and cancer biology: modulating signaling pathways for therapeutic intervention.Cancer Biol Ther. 2010; 10: 961-978Crossref PubMed Google Scholar The purpose of this review is to highlight the salient findings demonstrating how KSHV uses the pivotal COX-2/PGE2/EP receptor mediated inflammatory axis for its survival and pathogenesis and, therefore, plays a crucial role in KSHV-associated malignancies. COX or prostaglandin-endoperoxide synthase catalyzes the conversion of arachidonic acid (AA) into prostaglandin H2, which is further converted into the proinflammatory lipid metabolites such as PGE2, PGI2, PGF2, and thromboxane-2 by specific enzymes and play crucial roles in diverse physiological functions such as platelet aggregation, inhibition of gastrointestinal (GI) acid secretion, regulation of glomerular function, and labor.13Chandrasekharan N.V. Simmons D.L. The cyclooxygenases.Genome Biol. 2004; 5: 241Crossref PubMed Scopus (0) Google Scholar The COX-1 isoform has a constitutively active promoter whereas COX-2 has an inducible promoter activated by stress, growth factors, cytokines, and infections.13Chandrasekharan N.V. Simmons D.L. 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The cyclooxygenases.Genome Biol. 2004; 5: 241Crossref PubMed Scopus (0) Google Scholar The major lipid metabolite of COX-2 implicated in tumorigenesis is PGE2.19Wang D. Dubois R.N. Eicosanoids and cancer.Nat Rev Cancer. 2010; 10: 181-193Crossref PubMed Google Scholar PGE2 is an autocrine and paracrine lipid signal inducer with a circulating half-life of approximately 30 seconds and normal plasma levels varying from 3-15 pg/mL.20Fitzpatrick F.A. Aguirre R. Pike J.E. Lincoln F.H. The stability of 13,14-dihydro-15 keto-PGE2.Prostaglandins. 1980; 19: 917-931Crossref PubMed Google Scholar PGE2 exerts its effects through the 7-transmembrane rhodopsin family of G protein coupled (GPCR) eicosanoid (EP) receptors, namely, EP1, EP2, EP3, and EP4 (EP 1-4) that initiate signal transduction through Calcium (Ca)2+, Cyclic adenosine monophosphate (cAMP), protein kinase A (PKA), and Phosphatidylinositide 3-kinase (PI3K).5Wang D. Dubois R.N. 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Proinflammatory prostaglandins and progression of colorectal cancer.Cancer Lett. 2008; 267: 197-203Abstract Full Text Full Text PDF PubMed Google Scholar In recent years, the link between EP receptors and tumorigenesis had also revealed the possibility of using highly specific EP receptor antagonists such as SC-51322 (EP1 antagonist), AH6809 (EP2 antagonist), and AH23848 (EP4 antagonist) as anticancer drugs.25Casibang M. Moody T.W. AH6809 antagonizes nonsmall cell lung cancer prostaglandin receptors.Lung Cancer. 2002; 36: 33-42Abstract Full Text Full Text PDF PubMed Google Scholar, 26Fulton A.M. Ma X. Kundu N. Targeting prostaglandin E EP receptors to inhibit metastasis.Cancer Res. 2006; 66: 9794-9797Crossref PubMed Google Scholar, 27Majima M. Amano H. Hayashi I. Prostanoid receptor signaling relevant to tumor growth and angiogenesis.Trends Pharmacol Sci. 2003; 24: 524-529Abstract Full Text Full Text PDF PubMed Google Scholar Infections by several viruses have been shown to regulate COX-2 expression and PGE2 production such as HBV in hepatocytes,28Lara-Pezzi E. Gomez-Gaviro M.V. Galvez B.G. et al.The hepatitis B virus X protein promotes tumor cell invasion by inducing membrane-type matrix metalloproteinase-1 and cyclooxygenase-2 expression.J Clin Invest. 2002; 110: 1831-1838PubMed Google Scholar, 29Lim W. Kwon S.H. Cho H. et al.HBx targeting to mitochondria and ROS generation are necessary but insufficient for HBV-induced cyclooxygenase-2 expression.J Mol Med (Berl). 2011; 88: 359-369Crossref Google Scholar HCV in Huh-7 cells,30Waris G. Siddiqui A. Hepatitis C virus stimulates the expression of cyclooxygenase-2 via oxidative stress: role of prostaglandin E2 in RNA replication.J Virol. 2005; 79: 9725-9734Crossref PubMed Google Scholar human herpesvirus 6 (HHV-6) in monocytes,31Janelle M.E. Gravel A. Gosselin J. Tremblay M.J. Flamand L. Activation of monocyte cyclooxygenase-2 gene expression by human herpesvirus 6. Role for cyclic AMP-responsive element-binding protein and activator protein-1.J Biol Chem. 2002; 277: 30665-30674Crossref PubMed Google Scholar human cytomegalovirus (CMV) in Peripheral blood mononuclear cells (PBMCs), smooth muscle cells, and fibroblasts,32Nokta M.A. Hassan M.I. Loesch K. Pollard R.B. Human cytomegalovirus-induced immunosuppression. Relationship to tumor necrosis factor-dependent release of arachidonic acid and prostaglandin E2 in human monocytes.J Clin Invest. 1996; 97: 2635-2641Crossref PubMed Google Scholar, 33Speir E. Yu Z.X. Ferrans V.J. Huang E.S. Epstein S.E. Aspirin attenuates cytomegalovirus infectivity and gene expression mediated by cyclooxygenase-2 in coronary artery smooth muscle cells.Circ Res. 1998; 83: 210-216Crossref PubMed Google Scholar, 34Zhu H. Cong J.P. Yu D. Bresnahan W.A. Shenk T.E. Inhibition of cyclooxygenase 2 blocks human cytomegalovirus replication.Proc Natl Acad Sci U S A. 2002; 99: 3932-3937Crossref PubMed Scopus (0) Google Scholar, 35Schroer J. Shenk T. Inhibition of cyclooxygenase activity blocks cell-to-cell spread of human cytomegalovirus.Proc Natl Acad Sci U S A. 2008; 105: 19468-19473Crossref PubMed Google Scholar murine gammaherpesvirus 68 (MHV-68) in NIH 3T3 cells,36Symensma T.L. Martinez-Guzman D. Jia Q. et al.COX-2 induction during murine gammaherpesvirus 68 infection leads to enhancement of viral gene expression.J Virol. 2003; 77: 12753-12763Crossref PubMed Google Scholar HIV in monocytes,37Wahl L.M. Corcoran M.L. Pyle S.W. Arthur L.O. Harel-Bellan A. Farrar W.L. Human immunodeficiency virus glycoprotein (gp120) induction of monocyte arachidonic acid metabolites and interleukin 1.Proc Natl Acad Sci U S A. 1989; 86: 621-625Crossref PubMed Google Scholar, 38Foley P. Kazazi F. Biti R. Sorrell T.C. Cunningham A.L. HIV infection of monocytes inhibits the T-lymphocyte proliferative response to recall antigens, via production of eicosanoids.Immunology. 1992; 75: 391-397PubMed Google Scholar HTLV-1 in PBMCs,39Moriuchi M. Inoue H. Moriuchi H. Reciprocal interactions between human T-lymphotropic virus type 1 and prostaglandins: implications for viral transmission.J Virol. 2001; 75: 192-198Crossref PubMed Scopus (0) Google Scholar influenza virus in PBMCs,40Liu L. Li R. Pan Y. et al.High-throughput screen of protein expression levels induced by cyclooxygenase-2 during influenza a virus infection.Clin Chim Acta. 2011; 412: 1081-1085Crossref PubMed Google Scholar enterovirus 71 in human neuroblastoma cells,41Tung W.H. Hsieh H.L. Lee I.T. Yang C.M. Enterovirus 71 modulates a COX-2/PGE2/cAMP-dependent viral replication in human neuroblastoma cells: role of the c-Src/EGFR/p42/p44 MAPK/CREB signaling pathway.J Cell Biochem. 2011; 112: 559-570Crossref PubMed Google Scholar dengue virus in dendritic cells,42Wu W.L. Ho L.J. Chang D.M. Chen C.H. Lai J.H. Triggering of DC migration by dengue virus stimulation of COX-2-dependent signaling cascades in vitro highlights the significance of these cascades beyond inflammation.Eur J Immunol. 2009; 39: 3413-3422Crossref PubMed Google Scholar Severe acute respiratory syndrome (SARS)-associated coronavirus in 293T cells,43Yan X. Hao Q. Mu Y. et al.Nucleocapsid protein of SARS-CoV activates the expression of cyclooxygenase-2 by binding directly to regulatory elements for nuclear factor-kappa B and CCAAT/enhancer binding protein.Int J Biochem Cell Biol. 2006; 38: 1417-1428Crossref PubMed Scopus (0) Google Scholar Theiler's murine encephalomyelitis virus in astrocytes,44Molina-Holgado E. Arevalo-Martin A. Ortiz S. Vela J.M. Guaza C. Theiler's virus infection induces the expression of cyclooxygenase-2 in murine astrocytes: inhibition by the anti-inflammatory cytokines interleukin-4 and interleukin-10.Neurosci Lett. 2002; 324: 237-241Crossref PubMed Scopus (0) Google Scholar encephalomyocarditis virus in macrophages,45Steer S.A. Corbett J.A. The role and regulation of COX-2 during viral infection.Viral Immunol. 2003; 16: 447-460Crossref PubMed Google Scholar, 46Steer S.A. Moran J.M. Christmann B.S. Maggi Jr., L.B. Corbett J.A. Role of MAPK in the regulation of double-stranded RNA- and encephalomyocarditis virus-induced cyclooxygenase-2 expression by macrophages.J Immunol. 2006; 177: 3413-3420PubMed Google Scholar coxsackie virus B3 in monocytes,47Henke A. Spengler H.P. Stelzner A. Nain M. Gemsa D. Lipopolysaccharide suppresses cytokine release from coxsackie virus-infected human monocytes.Res Immunol. 1992; 143: 65-70Crossref PubMed Scopus (0) Google Scholar respiratory syncytial virus in macrophages and dendritic cells,48Bartz H. Buning-Pfaue F. Turkel O. Schauer U. Respiratory syncytial virus induces prostaglandin E2, IL-10 and IL-11 generation in antigen presenting cells.Clin Exp Immunol. 2002; 129: 438-445Crossref PubMed Scopus (0) Google Scholar and canine distemper virus in monocytes.49Krakowka S. Ringler S.S. Lewis M. Olsen R.G. Axthelm M.K. Immunosuppression by canine distemper virus: modulation of in vitro immunoglobulin synthesis, interleukin release and prostaglandin E2 production.Vet Immunol Immunopathol. 1987; 15: 181-201Crossref PubMed Google Scholar COX-2/PGE2 has been implicated in a multitude of viral mechanisms such as genome replication (HBV), (CMV, HTLV), gene expression (MHV-68), transmission (HTLV), cell tropism (rhesus CMV), cell invasion (CMV), T cell regulation (HIV), and even has identified a viral homologue of COX-2 in rhesus CMV revealing the significance of COX-2 in the evolution of inflammation mediated viral pathogenesis.28Lara-Pezzi E. Gomez-Gaviro M.V. Galvez B.G. et al.The hepatitis B virus X protein promotes tumor cell invasion by inducing membrane-type matrix metalloproteinase-1 and cyclooxygenase-2 expression.J Clin Invest. 2002; 110: 1831-1838PubMed Google Scholar, 29Lim W. Kwon S.H. Cho H. et al.HBx targeting to mitochondria and ROS generation are necessary but insufficient for HBV-induced cyclooxygenase-2 expression.J Mol Med (Berl). 2011; 88: 359-369Crossref Google Scholar, 30Waris G. Siddiqui A. Hepatitis C virus stimulates the expression of cyclooxygenase-2 via oxidative stress: role of prostaglandin E2 in RNA replication.J Virol. 2005; 79: 9725-9734Crossref PubMed Google Scholar, 31Janelle M.E. Gravel A. Gosselin J. Tremblay M.J. Flamand L. Activation of monocyte cyclooxygenase-2 gene expression by human herpesvirus 6. Role for cyclic AMP-responsive element-binding protein and activator protein-1.J Biol Chem. 2002; 277: 30665-30674Crossref PubMed Google Scholar, 32Nokta M.A. Hassan M.I. Loesch K. Pollard R.B. Human cytomegalovirus-induced immunosuppression. Relationship to tumor necrosis factor-dependent release of arachidonic acid and prostaglandin E2 in human monocytes.J Clin Invest. 1996; 97: 2635-2641Crossref PubMed Google Scholar, 33Speir E. Yu Z.X. Ferrans V.J. Huang E.S. Epstein S.E. Aspirin attenuates cytomegalovirus infectivity and gene expression mediated by cyclooxygenase-2 in coronary artery smooth muscle cells.Circ Res. 1998; 83: 210-216Crossref PubMed Google Scholar, 34Zhu H. Cong J.P. Yu D. Bresnahan W.A. Shenk T.E. Inhibition of cyclooxygenase 2 blocks human cytomegalovirus replication.Proc Natl Acad Sci U S A. 2002; 99: 3932-3937Crossref PubMed Scopus (0) Google Scholar, 35Schroer J. Shenk T. Inhibition of cyclooxygenase activity blocks cell-to-cell spread of human cytomegalovirus.Proc Natl Acad Sci U S A. 2008; 105: 19468-19473Crossref PubMed Google Scholar, 36Symensma T.L. Martinez-Guzman D. Jia Q. et al.COX-2 induction during murine gammaherpesvirus 68 infection leads to enhancement of viral gene expression.J Virol. 2003; 77: 12753-12763Crossref PubMed Google Scholar, 37Wahl L.M. Corcoran M.L. Pyle S.W. Arthur L.O. Harel-Bellan A. Farrar W.L. Human immunodeficiency virus glycoprotein (gp120) induction of monocyte arachidonic acid metabolites and interleukin 1.Proc Natl Acad Sci U S A. 1989; 86: 621-625Crossref PubMed Google Scholar, 38Foley P. Kazazi F. Biti R. Sorrell T.C. Cunningham A.L. HIV infection of monocytes inhibits the T-lymphocyte proliferative response to recall antigens, via production of eicosanoids.Immunology. 1992; 75: 391-397PubMed Google Scholar, 39Moriuchi M. Inoue H. Moriuchi H. Reciprocal interactions between human T-lymphotropic virus type 1 and prostaglandins: implications for viral transmission.J Virol. 2001; 75: 192-198Crossref PubMed Scopus (0) Google Scholar, 40Liu L. Li R. Pan Y. et al.High-throughput screen of protein expression levels induced by cyclooxygenase-2 during influenza a virus infection.Clin Chim Acta. 2011; 412: 1081-1085Crossref PubMed Google Scholar, 41Tung W.H. Hsieh H.L. Lee I.T. Yang C.M. Enterovirus 71 modulates a COX-2/PGE2/cAMP-dependent viral replication in human neuroblastoma cells: role of the c-Src/EGFR/p42/p44 MAPK/CREB signaling pathway.J Cell Biochem. 2011; 112: 559-570Crossref PubMed Google Scholar, 42Wu W.L. Ho L.J. Chang D.M. Chen C.H. Lai J.H. Triggering of DC migration by dengue virus stimulation of COX-2-dependent signaling cascades in vitro highlights the significance of these cascades beyond inflammation.Eur J Immunol. 2009; 39: 3413-3422Crossref PubMed Google Scholar, 43Yan X. Hao Q. Mu Y. et al.Nucleocapsid protein of SARS-CoV activates the expression of cyclooxygenase-2 by binding directly to regulatory elements for nuclear factor-kappa B and CCAAT/enhancer binding protein.Int J Biochem Cell Biol. 2006; 38: 1417-1428Crossref PubMed Scopus (0) Google Scholar, 44Molina-Holgado E. Arevalo-Martin A. Ortiz S. Vela J.M. Guaza C. Theiler's virus infection induces the expression of cyclooxygenase-2 in murine astrocytes: inhibition by the anti-inflammatory cytokines interleukin-4 and interleukin-10.Neurosci Lett. 2002; 324: 237-241Crossref PubMed Scopus (0) Google Scholar, 45Steer S.A. Corbett J.A. The role and regulation of COX-2 during viral infection.Viral Immunol. 2003; 16: 447-460Crossref PubMed Google Scholar, 47Henke A. Spengler H.P. Stelzner A. Nain M. Gemsa D. Lipopolysaccharide suppresses cytokine release from coxsackie virus-infected human monocytes.Res Immunol. 1992; 143: 65-70Crossref PubMed Scopus (0) Google Scholar, 48Bartz H. Buning-Pfaue F. Turkel O. Schauer U. Respiratory syncytial virus induces prostaglandin E2, IL-10 and IL-11 generation in antigen presenting cells.Clin Exp Immunol. 2002; 129: 438-445Crossref PubMed Scopus (0) Google Scholar, 49Krakowka S. Ringler S.S. Lewis M. Olsen R.G. Axthelm M.K. Immunosuppression by canine distemper virus: modulation of in vitro immunoglobulin synthesis, interleukin release and prostaglandin E2 production.Vet Immunol Immunopathol. 1987; 15: 181-201Crossref PubMed Google Scholar, 50Reynolds A.E. Enquist L.W. Biological interactions between herpesviruses and cyclooxygenase enzymes.Rev Med Virol. 2006; 16: 393-403Crossref PubMed Google Scholar, 51Rue C.A. Jarvis M.A. Knoche A.J. et al.A cyclooxygenase-2 homologue encoded by rhesus cytomegalovirus is a determinant for endothelial cell tropism.J Virol. 2004; 78: 12529-12536Crossref PubMed Scopus (0) Google Scholar Among the herpes viruses, studies using COX inhibitors have shown the role of COX-2/PGE2 pathways for replication and successful lytic cycle in HSV, CMV, HHV-6, and MHV-68.31Janelle M.E. Gravel A. Gosselin J. Tremblay M.J. Flamand L. Activation of monocyte cyclooxygenase-2 gene expression by human herpesvirus 6. Role for cyclic AMP-responsive element-binding protein and activator protein-1.J Biol Chem. 2002; 277: 30665-30674Crossref PubMed Google Scholar, 34Zhu H. Cong J.P. Yu D. Bresnahan W.A. Shenk T.E. Inhibition of cyclooxygenase 2 blocks human cytomegalovirus replication.Proc Natl Acad Sci U S A. 2002; 99: 3932-3937Crossref PubMed Scopus (0) Google Scholar, 35Schroer J. Shenk T. Inhibition of cyclooxygenase activity blocks cell-to-cell spread of human cytomegalovirus.Proc Natl Acad Sci U S A. 2008; 105: 19468-19473Crossref PubMed Google Scholar, 36Symensma T.L. Martinez-Guzman D. Jia Q. et al.COX-2 induction during murine gammaherpesvirus 68 infection leads to enhancement of viral gene expression.J Virol. 2003; 77: 12753-12763Crossref PubMed Google Scholar, 51Rue C.A. Jarvis M.A. Knoche A.J. et al.A cyclooxygenase-2 homologue encoded by rhesus cytomegalovirus is a determinant for endothelial cell tropism.J Virol. 2004; 78: 12529-12536Crossref PubMed Scopus (0) Google Scholar, 52Kaul R. Verma S.C. Murakami M. Lan K. Choudhuri T. Robertson E.S. Epstein-Barr virus protein can
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