scholarly journals Spontaneous Loss of Viral Episomes Accompanying Epstein‐Barr Virus Reactivation in a Burkitt's Lymphoma Cell Line

1998 ◽  
Vol 177 (6) ◽  
pp. 1705-1709 ◽  
Author(s):  
Shamala K. Srinivas ◽  
Jeffery T. Sample ◽  
John W. Sixbey
Keyword(s):  
Cell Line ◽  
Epstein Barr Virus ◽  
Burkitt’S Lymphoma ◽  
Lymphoma Cell ◽  
Burkitt's Lymphoma ◽  
Lymphoma Cell Line ◽  
Virus Reactivation ◽  
Barr Virus ◽  
Epstein Barr ◽  
Epstein Barr Virus Reactivation

scholarly journals The bfl-1 Gene Is Transcriptionally Upregulated by the Epstein-Barr Virus LMP1, and Its Expression Promotes the Survival of a Burkitt's Lymphoma Cell Line

2000 ◽  
Vol 74 (14) ◽  
pp. 6652-6658 ◽  
Author(s):  
Brendan D'Souza ◽  
Martin Rowe ◽  
Dermot Walls
Keyword(s):  
Cell Line ◽  
Cell Lines ◽  
Epstein Barr Virus ◽  
Burkitt’S Lymphoma ◽  
Lymphoma Cell ◽  
Burkitt's Lymphoma ◽  
Type I ◽  
Lymphoma Cell Line ◽  
Barr Virus ◽  
Epstein Barr

ABSTRACT The recently identified bfl-1 gene (also known asA1 or GRS), a homologue of bcl-2, encodes an antiapoptotic protein that suppresses apoptosis induced by the p53 tumor suppressor protein and exhibits proliferative and potent cooperative transforming activities. We show that elevated levels of bfl-1 mRNA are a feature of Epstein-Barr virus (EBV)-immortalized B-cell lines and Burkitt's lymphoma cell lines expressing the full spectrum of EBV latent proteins. Using an EBV-negative Burkitt's lymphoma cell line in which the expression of EBV latent membrane protein 1 (LMP1) is inducibly regulated by tetracycline, we demonstrate that LMP1 expression coincides with a dramatic increase in the level ofbfl-1 mRNA. Also in this system, an increase in the level of Bcl-2 protein was seen to occur earlier than that ofbcl-2 mRNA, suggesting that both transcriptional and translational mechanisms are involved in the control of Bcl-2 expression by LMP-1. We show that elevated bfl-1mRNA stability can contribute to this effect of LMP-1, thus providing evidence of a novel mechanism of gene regulation by this EBV protein. Upregulation ofbfl-1 by LMP1 was not observed in the T-cell line Jurkat or the epithelial cell line C33A. Ectopic expression of Bfl-1 in an EBV-positive cell line exhibiting a latency type I infection protects against apoptosis induced by growth factor deprivation, thereby providing a functional role for Bfl-1 in this cellular context and adding Bfl-1 to the list of antiapoptotic proteins whose expression is modulated by EBV. This is the first report of the regulation of bfl-1expression by a viral protein, and this novel finding may thus represent an important link between the EBV oncoprotein LMP1 and its cellular growth-transforming properties.

scholarly journals Role of bcl-2 in Epstein-Barr Virus-Induced Malignant Conversion of Burkitt's Lymphoma Cell Line Akata

2001 ◽  
Vol 75 (3) ◽  
pp. 1561-1564 ◽  
Author(s):  
Jun Komano ◽  
Kenzo Takada
Keyword(s):  
Cell Line ◽  
Scid Mouse ◽  
Epstein Barr Virus ◽  
Burkitt’S Lymphoma ◽  
Lymphoma Cell ◽  
Burkitt's Lymphoma ◽  
Lymphoma Cell Line ◽  
Barr Virus ◽  
Epstein Barr ◽  
Soft Agarose

ABSTRACT We have demonstrated that Epstein-Barr virus (EBV) confers enhanced growth capability in soft agarose, tumorigenesis in the SCID mouse, and resistance to apoptosis in the Burkitt's lymphoma cell line Akata. Subsequently, we have shown that EBV-encoded small RNAs (EBERs) are responsible for these phenotypes. We constantly observed the upregulation of bcl-2 oncoprotein expression upon EBV infection and expression of EBERs. To test whether these phenotypes were due to the upregulation of bcl-2 expression, we introduced bcl-2 into EBV-negative Akata cells at various levels encompassing the range at which EBV-positive cells expressed it. As cells expressed bcl-2 at higher levels, they became more capable of growing in soft agarose and became resistant to apoptosis. However, clones expressing bcl-2 at a higher level than EBV-positive Akata cells were negative in the tumorigenesis assay in the SCID mouse. On the other hand, introduction of bax into EBV-positive Akata cells reduced the resistance to apoptosis; however, it failed to reduce the growth capability in soft agarose. These data indicate that EBV targets not only bcl-2, but also an unknown pathway(s) to enhance the oncogenic potential of Akata cells.

scholarly journals Accumulation of Epstein–Barr virus (EBV) BMRF1 protein EA-D during latent EBV activation of Burkitt's lymphoma cell line Raji

2007 ◽  
Vol 9 (2) ◽  
pp. 150-159 ◽  
Author(s):  
Makoto Ohashi ◽  
Kazutaka Horie ◽  
Yoshiko Hoshikawa ◽  
Keiko Nagata ◽  
Mistuhiko Osaki ◽  
...  
Keyword(s):  
Cell Line ◽  
Epstein Barr Virus ◽  
Burkitt’S Lymphoma ◽  
Lymphoma Cell ◽  
Burkitt's Lymphoma ◽  
Lymphoma Cell Line ◽  
Barr Virus ◽  
Epstein Barr
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