دورية أكاديمية

Epstein-Barr virus infection alters cellular signal cascades in human nasopharyngeal epithelial cells.

التفاصيل البيبلوغرافية
العنوان: Epstein-Barr virus infection alters cellular signal cascades in human nasopharyngeal epithelial cells.
المؤلفون: Lo AK; Department of Anatomical and Cellular Pathology, Prince of Wales Hospital, The Chinese University of Hong Kong, Shatin, Hong Kong SAR, China., Lo KW, Tsao SW, Wong HL, Hui JW, To KF, Hayward DS, Chui YL, Lau YL, Takada K, Huang DP
المصدر: Neoplasia (New York, N.Y.) [Neoplasia] 2006 Mar; Vol. 8 (3), pp. 173-80.
نوع المنشور: Journal Article; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: Elsevier Country of Publication: United States NLM ID: 100886622 Publication Model: Print Cited Medium: Internet ISSN: 1476-5586 (Electronic) Linking ISSN: 14765586 NLM ISO Abbreviation: Neoplasia Subsets: MEDLINE
أسماء مطبوعة: Publication: 2014- : [Amsterdam] : Elsevier
Original Publication: New York, NY : Stockton Press, c1999-
مواضيع طبية MeSH: Cell Transformation, Viral* , Signal Transduction*, Carcinoma/*pathology , Epithelial Cells/*virology , Epstein-Barr Virus Infections/*physiopathology , Herpesvirus 4, Human/*physiology , Nasopharyngeal Neoplasms/*pathology , Nasopharynx/*cytology, Carcinoma/immunology ; Carcinoma/virology ; Cell Line/physiology ; Cell Line/virology ; Cell Line, Tumor ; Cytokines/biosynthesis ; Cytokines/genetics ; Epithelial Cells/physiology ; Gene Expression Regulation, Neoplastic ; Gene Expression Regulation, Viral ; Humans ; Inflammation ; MAP Kinase Signaling System ; NF-kappa B/physiology ; Nasopharyngeal Neoplasms/immunology ; Nasopharyngeal Neoplasms/virology ; Neoplasm Proteins/biosynthesis ; Neoplasm Proteins/genetics ; Phosphorylation ; Protein Processing, Post-Translational ; Reverse Transcriptase Polymerase Chain Reaction ; STAT3 Transcription Factor/physiology ; Virus Latency ; eIF-2 Kinase/physiology
مستخلص: Epstein-Barr virus (EBV) latent infection is a critical event in nasopharyngeal carcinoma (NPC) tumorigenesis. EBV-encoded genes have been shown to be involved in immune evasion and in the regulation of various cellular signaling cascades. To elucidate the roles of EBV in NPC development, stable infection of EBV in nasopharyngeal epithelial cell lines was established. Similar to primary tumors of NPC, these infected cells exhibited a type II EBV latency expression pattern. In this study, multiple cellular signaling pathways in EBV-infected cells were investigated. We first demonstrated that in vitro EBV infection resulted in the activation of STAT3 and NFkappaB signal cascades in nasopharyngeal epithelial cells. Increased expression of their downstream targets (c-Myc, Bcl-xL, IL-6, LIF, SOCS-1, SOCS-3, VEGF, and COX-2) was also observed. Moreover, EBV latent infection induced the suppression of p38-MAPK activities, but did not activate PKR cascade. Our findings suggest that EBV latent infection is able to manipulate multiple cellular signal cascades to protect infected cells from immunologic attack and to facilitate cancer development.
References: Int J Cancer. 1999 Sep 24;83(1):121-6. (PMID: 10449618)
Lab Invest. 1993 Jun;68(6):716-27. (PMID: 7685844)
Proc Natl Acad Sci U S A. 2001 Jun 5;98(12):6905-10. (PMID: 11381123)
Oncogene. 2004 Nov 11;23(53):8619-28. (PMID: 15361852)
J Virol. 2003 Apr;77(7):4139-48. (PMID: 12634372)
Oncogene. 2002 Mar 27;21(13):2000-8. (PMID: 11960372)
Nat Rev Cancer. 2004 Oct;4(10):757-68. (PMID: 15510157)
Cytokine Growth Factor Rev. 2004 Dec;15(6):435-55. (PMID: 15561601)
J Virol. 1998 May;72(5):4371-8. (PMID: 9557727)
Laryngoscope. 2000 Dec;110(12):2066-9. (PMID: 11129022)
J Virol. 2000 Nov;74(22):10681-9. (PMID: 11044112)
Lab Invest. 2003 May;83(5):697-709. (PMID: 12746479)
Cancer Res. 2000 Oct 1;60(19):5365-70. (PMID: 11034072)
Int J Cancer. 2004 May 10;109(6):919-25. (PMID: 15027126)
Mol Carcinog. 2005 Oct;44(2):92-101. (PMID: 16086371)
Oncogene. 2000 May 15;19(21):2548-56. (PMID: 10851053)
J Virol. 1999 Oct;73(10):8857-66. (PMID: 10482644)
Br J Cancer. 2003 Jul 21;89(2):344-9. (PMID: 12865928)
Oncogene. 2000 May 15;19(21):2474-88. (PMID: 10851046)
EMBO J. 2002 Mar 1;21(5):954-65. (PMID: 11867523)
Cancer Cell. 2004 May;5(5):423-8. (PMID: 15144950)
Proc Natl Acad Sci U S A. 2003 Feb 18;100(4):1879-84. (PMID: 12571365)
J Clin Invest. 2004 Sep;114(5):720-8. (PMID: 15343391)
Biochim Biophys Acta. 2002 Jun 12;1590(1-3):150-8. (PMID: 12063178)
Leukemia. 2005 Feb;19(2):209-13. (PMID: 15618960)
Nat Med. 2004 Jan;10(1):48-54. (PMID: 14702634)
J Gen Virol. 2001 Oct;82(Pt 10):2373-2383. (PMID: 11562531)
Oncogene. 2003 Aug 11;22(33):5108-21. (PMID: 12910248)
Int J Cancer. 1980 Aug;26(2):127-32. (PMID: 6259064)
المشرفين على المادة: 0 (Cytokines)
0 (NF-kappa B)
0 (Neoplasm Proteins)
0 (STAT3 Transcription Factor)
0 (STAT3 protein, human)
EC 2.7.11.1 (eIF-2 Kinase)
تواريخ الأحداث: Date Created: 20060414 Date Completed: 20060831 Latest Revision: 20220410
رمز التحديث: 20240628
مُعرف محوري في PubMed: PMC1578522
DOI: 10.1593/neo.05625
PMID: 16611410
قاعدة البيانات: MEDLINE
الوصف
تدمد:1476-5586
DOI:10.1593/neo.05625