Establishment of Epstein-Barr virus (EBV)-associated nuclear antigen (EBNA)-positive nasopharyngeal carcinoma hybrid cell line (NPC-KT)

1984 ◽  
Vol 239 (1) ◽  
pp. 87-92 ◽  
Author(s):  
T. Takimoto ◽  
M. Kamide ◽  
R. Umeda
Keyword(s):  
Nasopharyngeal Carcinoma ◽  
Cell Line ◽  
Epstein Barr Virus ◽  
Hybrid Cell ◽  
Hybrid Cell Line ◽  
Nuclear Antigen ◽  
Barr Virus ◽  
Epstein Barr

Epstein-Barr Virus Lytic Cycle Spreads Via Cell Fusion in a Nasopharyngeal Carcinoma Hybrid Cell Line

1994 ◽  
Vol 104 (1) ◽  
pp. 91???94 ◽  
Author(s):  
Tomokazu Yoshizaki ◽  
Toru Takimoto ◽  
Hazime Takeshita ◽  
Saichiro Tanaka ◽  
Mitsuru Furukawa ◽  
...  
Keyword(s):  
Nasopharyngeal Carcinoma ◽  
Cell Line ◽  
Cell Fusion ◽  
Epstein Barr Virus ◽  
Hybrid Cell ◽  
Lytic Cycle ◽  
Hybrid Cell Line ◽  
Barr Virus ◽  
Epstein Barr

Effects of Chemical Inducers on the Epstein-Barr Virus Cycle in Epithelial/Nasopharyngeal Carcinoma Hybrid Cell Line

ORL ◽  
1984 ◽  
Vol 46 (4) ◽  
pp. 192-194 ◽  
Author(s):  
T. Takimoto ◽  
H. Ishiguro ◽  
R. Umeda ◽  
H. Ogura ◽  
M. Hatano
Keyword(s):  
Nasopharyngeal Carcinoma ◽  
Cell Line ◽  
Epstein Barr Virus ◽  
Hybrid Cell ◽  
Hybrid Cell Line ◽  
Chemical Inducers ◽  
Barr Virus ◽  
Epstein Barr

scholarly journals Mechanisms of Epstein‐Barr virus nuclear antigen 1 favor Tregs accumulation in nasopharyngeal carcinoma

2020 ◽  
Vol 9 (15) ◽  
pp. 5598-5608
Author(s):  
Jie Wang ◽  
Yunfan Luo ◽  
Pei Bi ◽  
Juan Lu ◽  
Fan Wang ◽  
...  
Keyword(s):  
Nasopharyngeal Carcinoma ◽  
Epstein Barr Virus ◽  
Nuclear Antigen ◽  
Barr Virus ◽  
Epstein Barr

scholarly journals Curcumin Inhibits Proliferation of Epstein–Barr Virus-Associated Human Nasopharyngeal Carcinoma Cells by Inhibiting EBV Nuclear Antigen 1 Expression

2019 ◽  
Vol 2019 ◽  
pp. 1-10
Author(s):  
Limei Liu ◽  
Jiaomin Yang ◽  
Wuguang Ji ◽  
Chao Wang
Keyword(s):  
Nasopharyngeal Carcinoma ◽  
Epstein Barr Virus ◽  
Lytic Replication ◽  
Nuclear Antigen ◽  
Mrna Levels ◽  
Curcumin Treatment ◽  
Antitumor Effects ◽  
Barr Virus ◽  
Cycle Arrest ◽  
Epstein Barr

This investigation aims to study the effect of curcumin on the proliferation, cycle arrest, and apoptosis of Epstein–Barr virus- (EBV-) positive nasopharyngeal carcinoma (NPC) cells. EBV+ NPC cells were subjected to curcumin treatment. The cell viability was evaluated with the CCK-8. Cell cycle and apoptosis were analyzed by flow cytometry analysis. Expression (protein and mRNA) levels were detected with western blotting and quantitative real-time PCR, respectively. Curcumin efficiently reduced the viability of EBV+ NPC cells. Curcumin induced the cycle arrest of the HONE1 and HK1-EBV cells positive for EBV. Moreover, curcumin treatment promoted the NPC cell apoptosis, via the mitochondria- and death receptor-mediated pathways. Furthermore, curcumin decreased the expression of EBNA1 in the HONE1 and HK1-EBV cells and inhibited the transcriptional level of EBNA1 in the HeLa cells. Curcumin induced EBNA1 degradation via the proteasome-ubiquitin pathway. In addition, curcumin inhibited the proliferation of HONE1 and HK1-EBV cells positive for EBV, probably by decreasing the expression level of EBNA1. In both the HONE1 and HK1-EBV cells, curcumin inhibited the EBV latent and lytic replication. Curcumin could reduce the EBNA1 expression and exert antitumor effects against NPC in vitro.

scholarly journals Establishment and characterization of an Epstein-Barr virus transformed cell line with strong phagocytic activity

Blood ◽  
1989 ◽  
Vol 74 (1) ◽  
pp. 430-436 ◽  
Author(s):  
P von den Driesch ◽  
R Bhardwaj ◽  
HD Flad ◽  
DC Neugebauer ◽  
HJ Pielken ◽  
...  
Keyword(s):  
Cell Line ◽  
Phagocytic Activity ◽  
Antigen Processing ◽  
Epstein Barr Virus ◽  
Interleukin 1 ◽  
Immunoglobulin M ◽  
Nuclear Antigen ◽  
Barr Virus ◽  
Transformed Cell Line ◽  
Epstein Barr

Abstract An immunoglobulin M (IgM)-positive cell line, Ms 28, apparently spontaneously transformed by Epstein-Barr virus (EBV) was established from peripheral blood cells of a patient with immature myeloblastic leukemia. It has been characterized according to phenotype, cytochemistry, and membrane antigen pattern. The cell line expresses lymphoid markers like CD 19, CD 22, and CD 30 and synthesizes and secretes IgM. Monocyte markers CD 11c, CD 14, and CD 15 are absent. Neither interleukin-1 (IL-1), nor tumor necrosis factor (TNF-alpha) are produced. But Ms 28 cells show strong phagocytic activity and engulf Latex particles and sheep RBCs (SRBCs) that need not to be opsonized. The phagocytic activity can be inhibited by chloroquine. Both phagocytosis and EBV nuclear-antigen (EBNA) expression can be observed in one and the same cell. Ms 28 cells might be useful to study immunologic activities like antigen processing and presentation.

scholarly journals Characterization of naturally Epstein–Barr virus-infected gastric carcinoma cell line YCCEL1

2013 ◽  
Vol 94 (3) ◽  
pp. 497-506 ◽  
Author(s):  
Do Nyun Kim ◽  
Min Koo Seo ◽  
Hoyun Choi ◽  
Su Yeon Kim ◽  
Hee Jong Shin ◽  
...  
Keyword(s):  
Cell Line ◽  
Cell Lines ◽  
Blot Analysis ◽  
Epstein Barr Virus ◽  
Model Systems ◽  
Nuclear Antigen ◽  
Gastric Carcinoma Cell ◽  
Barr Virus ◽  
Epstein Barr

Epstein–Barr virus (EBV) is a herpesvirus associated with lymphomas and carcinomas. While EBV-associated epithelial cell lines are good model systems to investigate the role of EBV in carcinoma, only a few cell lines are available as they are hard to acquire. A greater variety of naturally EBV-infected cell lines which are derived from tumour patients are needed to represent various features of EBVaGC. We characterized cell line YCCEL1, established from a Korean EBVaGC patient, to ascertain whether it can be used to study the roles of EBV in EBVaGC. The expression of EBV genes and cell surface markers was examined by in situ hybridization, RT-PCR, Western blot analysis, immunofluorescence assay and Northern blot analysis. EBV episomal status was analysed by Southern blotting and real-time PCR. This cell line expressed EBV nuclear antigen 1 (EBNA1) and latent membrane protein 2A (LMP2A), but not EBNA2, LMP2B nor LMP1. The majority of the lytic proteins were not detected in YCCEL1 cells either before or after treatment with 12-O-tetradecanoylphorbol-13-acetate. YCCEL1 cells expressed BART microRNAs (miRNAs) at high level but did not express BHRF1 miRNAs. YCCEL1 cells expressed cytokeratin, but not CD21 and CD19, suggesting CD21-independent EBV infection. The latent EBV gene and EBV miRNA expression pattern of YCCEL1 cells closely resembled that of general EBVaGC cases. Our results support the value of YCCEL1 cells as a good model system to study the role of EBV in gastric carcinogenesis.

scholarly journals Tumor microenvironment contributes to Epstein-Barr virus anti-nuclear antigen-1 antibody production in nasopharyngeal carcinoma

2017 ◽  
Vol 14 (2) ◽  
pp. 2458-2462 ◽  
Author(s):  
Ping Ai ◽  
Zhiping Li ◽  
Yong Jiang ◽  
Changping Song ◽  
Lin Zhang ◽  
...  
Keyword(s):  
Nasopharyngeal Carcinoma ◽  
Tumor Microenvironment ◽  
Antibody Production ◽  
Epstein Barr Virus ◽  
Nuclear Antigen ◽  
Barr Virus ◽  
Epstein Barr

scholarly journals Epstein-Barr Virus EBNA-3C Is Targeted to and Regulates Expression from the Bidirectional LMP-1/2B Promoter

2006 ◽  
Vol 80 (22) ◽  
pp. 11200-11208 ◽  
Author(s):  
Carmilia Jiménez-Ramírez ◽  
Andrew J. Brooks ◽  
Linus Plym Forshell ◽  
Konstantin Yakimchuk ◽  
Bo Zhao ◽  
...  
Keyword(s):  
Cell Line ◽  
Epstein Barr Virus ◽  
Normal Growth ◽  
Growth Conditions ◽  
Nuclear Antigen ◽  
Regulation Of Transcription ◽  
Gene Promoters ◽  
Viral Oncoprotein ◽  
Barr Virus ◽  
Epstein Barr

ABSTRACT Epstein-Barr virus (EBV) nuclear antigen 3C (EBNA-3C) is essential for EBV-mediated immortalization of human B lymphocytes and regulates both the cell cycle and transcription. Transient reporter gene assays have implicated a pivotal role for EBNA-3C in the regulation of transcription of the majority of latency-associated genes expressed during the EBV growth program, including the viral oncoprotein LMP-1. To examine the regulation of latency gene expression by EBNA-3C, we generated an EBV-positive cell line that inducibly expresses EBNA-3C. This cell line allowed us to examine expression from the endogenous latency gene promoters in the context of an actual latent infection and the presence of other EBNA proteins, in particular EBNA-2, which is presumed to coregulate transcription with EBNA-3C. EBNA-3C induced the expression of both LMP-1 and LMP-2B mRNAs from the bidirectional LMP-1/LMP-2B promoter. In contrast, no effect was seen on expression from the common EBNA promoter Cp, which is responsive to EBNA-3C in reporter assays. Activation of LMP expression was not the consequence of increases in EBNA-2, PU.1 or Spi-B transcription factors, all of which are believed to be critical for activation of LMP-1. Chromatin immunoprecipitation assays furthermore indicated that EBNA-3C is present at the bidirectional LMP-1/LMP-2B promoter. These results indicate that EBNA-3C directly activates the expression of LMP-1 and LMP-2B but is unlikely to significantly regulate EBNA expression via Cp under normal growth conditions.

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