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Titolo:
Linkage between STAT regulation and Epstein-Barr virus gene expression in tumors
Autore:
Chen, HL; Lee, JM; Zong, YS; Borowitz, M; Ng, MH; Ambinder, RF; Hayward, SD;
Indirizzi:
Johns Hopkins Univ, Sch Med, Ctr Oncol, Baltimore, MD 21231 USA Johns Hopkins Univ Baltimore MD USA 21231 Oncol, Baltimore, MD 21231 USA Johns Hopkins Univ, Sch Med, Dept Pathol, Baltimore, MD 21231 USA Johns Hopkins Univ Baltimore MD USA 21231 Pathol, Baltimore, MD 21231 USA Sun Yat Sen Univ Med Sci, Guangzhou, Peoples R China Sun Yat Sen Univ Med Sci Guangzhou Peoples R China hou, Peoples R China Univ Hong Kong, Dept Microbiol, Hong Kong, Hong Kong, Peoples R China UnivHong Kong Hong Kong Hong Kong Peoples R China Kong, Peoples R China
Titolo Testata:
JOURNAL OF VIROLOGY
fascicolo: 6, volume: 75, anno: 2001,
pagine: 2929 - 2937
SICI:
0022-538X(200103)75:6<2929:LBSRAE>2.0.ZU;2-9
Fonte:
ISI
Lingua:
ENG
Soggetto:
NF-KAPPA-B; EPIDERMAL GROWTH-FACTOR; LATENT MEMBRANE-PROTEIN-1 ENGAGES; NUCLEAR ANTIGEN EBNA-1; LYMPHOMA CELL-LINES; CONSTITUTIVE ACTIVATION; FACTOR RECEPTOR; EPITHELIAL-CELLS; GERMINAL CENTER; DNA-BINDING;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
63
Recensione:
Indirizzi per estratti:
Indirizzo: Hayward, SD Johns Hopkins Univ, Sch Med, Ctr Oncol, 1650 Orleans St, Baltimore, MD 21231 USA Johns Hopkins Univ 1650 Orleans St Baltimore MD USA 21231 USA
Citazione:
H.L. Chen et al., "Linkage between STAT regulation and Epstein-Barr virus gene expression in tumors", J VIROLOGY, 75(6), 2001, pp. 2929-2937

Abstract

Epstein-Barr virus (EBV) latency gene expression in lymphoblastoid cell lines is regulated by EBNA2. However, the factors regulating viral expressionin EBV-associated tumors that do not express EBNA2 are poorly understood. In EBV-associated tumors, EBNA1 and frequently LMP1 are synthesized. We found that an alternative latent membrane protein 1 (LMP1) promoter, L1-TR, located within the terminal repeats is active in both nasopharyngeal carcinoma and Hodgkin's disease tissues. Examination of the L1-TR and the standard ED-L1 LMP1 promoters in electrophoretic mobility shift assays revealed thatboth promoters contain functional STAT binding sites. Further, both LMP1 promoters responded in reporter assays to activation of JAK-STAT signaling. Cotransfection of JAK1 or v-Src or treatment of cells with the cytokine interleukin-6 upregulated expression from ED-L1 and L1-TR reporter plasmids. Cotransfection of a dominant negative STAT3 beta revealed that STAT3 is likely to be the biologically relevant STAT for EBNA1 Qp and LMP1 L1-TR promoter regulation. In contrast, LMP1 expression from ED-L1 was not abrogated by STAT3 beta, indicating that the two LMP1 promoters are regulated by different STAT family members. Taken together with the previous demonstration of JAK-STAT activation of Qp driven EBNA1 expression, this places two of the EBV genes most commonly expressed in tumors under the control of the same signal transduction pathway. Immunohistochemical analyses of nasopharyngeal carcinoma tumors revealed that STAT3, STAT5, and STAT1 are constitutively activated in these tumors while STAT3 is constitutively activated in the malignant cells of Hodgkin's disease. We hypothesize that chronic or aberrant STAT activation may be both a necessary and predisposing event for EBV-driventumorigenesis in immunocompetent individuals.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 15/07/20 alle ore 08:33:55