scholarly journals Interference of Fisetin with Targets of the Nuclear Factor-κB Signal Transduction Pathway Activated by Epstein-Barr Virus Encoded Latent Membrane Protein 1

2014 ◽  
Vol 15 (22) ◽  
pp. 9835-9839 ◽  
Author(s):  
Rong Li ◽  
Hong-Ying Liang ◽  
Ming-Yong Li ◽  
Chun-Yan Lin ◽  
Meng-Jie Shi ◽  
...  
Keyword(s):  
Signal Transduction ◽  
Epstein Barr Virus ◽  
Signal Transduction Pathway ◽  
Nuclear Factor Κb ◽  
Latent Membrane Protein ◽  
Latent Membrane Protein 1 ◽  
Nuclear Factor ◽  
Transduction Pathway ◽  
Barr Virus ◽  
Epstein Barr

The latent membrane protein 1 (LMP1) encoded by Epstein-Barr virus induces expression of the putative oncogene Bcl-3 through activation of the nuclear factor-κB

2008 ◽  
Vol 131 (2) ◽  
pp. 170-179 ◽  
Author(s):  
Hiroyuki Nakamura ◽  
Chihiro Ishii ◽  
Masakazu Suehiro ◽  
Akifumi Iguchi ◽  
Kazumichi Kuroda ◽  
...  
Keyword(s):  
Membrane Protein ◽  
Epstein Barr Virus ◽  
Nuclear Factor Κb ◽  
Latent Membrane Protein ◽  
Latent Membrane Protein 1 ◽  
Nuclear Factor ◽  
Barr Virus ◽  
Epstein Barr

CD99 expression is positively regulated by Sp1 and is negatively regulated by Epstein-Barr virus latent membrane protein 1 through nuclear factor-κB

Blood ◽  
2001 ◽  
Vol 97 (11) ◽  
pp. 3596-3604 ◽  
Author(s):  
Im-soon Lee ◽  
Min Kyung Kim ◽  
Eun Young Choi ◽  
Anja Mehl ◽  
Kyeong Cheon Jung ◽  
...  
Keyword(s):  
Membrane Protein ◽  
Promoter Region ◽  
Promoter Activity ◽  
Epstein Barr Virus ◽  
Latent Membrane Protein ◽  
Hodgkin Disease ◽  
Latent Membrane Protein 1 ◽  
Nuclear Factor ◽  
Barr Virus ◽  
Epstein Barr

Epstein-Barr virus (EBV)–encoded latent membrane protein-1 (LMP1) is highly expressed in Hodgkin and Reed-Sternberg (H-RS) cells from patients with EBV-associated Hodgkin disease. It was previously demonstrated that CD99 can be negatively regulated by LMP1 at the transcriptional level, and the decreased expression of CD99 in a B lymphocyte cell line generates H-RS–like cells. In this study, detailed dissection of the CD99 promoter region was performed to search regulatory factor(s) involved in the expression of the gene. Using various mutant constructs containing deletions in the promoter region, it was revealed that the maximal promoter activity was retained on 5′-deletion to the position −137 from the transcriptional initiation site. Despite the presence of multiple putative Sp1-binding sites in the promoter region, the site located at −95 contributes heavily as a positive cis-acting element to its basal promoter activity. However, on examination of the involvement of the positive-acting Sp1-binding site of the promoter for the repressive activity of LMP1, it appeared to be dispensable. Instead, the repressive effect was mapped to the nuclear factor (NF)-κB activation domains in the cytoplasmic carboxyl terminus of LMP1 despite the absence of the NF-κB consensus sequences in the CD99 promoter region. Furthermore, the decreased CD99 promoter activity by LMP1 was markedly restored when NF-κB activity was inhibited. Taken together, these data suggest that Sp1 activates, whereas LMP1 represses, transcription from the CD99 promoter through the NF-κB signaling pathway, and they might aid in the understanding of the molecular mechanisms of viral pathogenesis in EBV-positive Hodgkin disease.

Silymarin Inhibits Proliferation and Induces Apoptosis in Epstein-Barr Virus-Positive Lymphoma Cells by Suppressing Nuclear Factor-Kappa B�Pathway

2020 ◽  
Vol 18 (4) ◽  
pp. 348-353
Author(s):  
Suli Lu ◽  
Jun Zhang ◽  
Yue Wang
Keyword(s):  
Cell Proliferation ◽  
Membrane Protein ◽  
Epstein Barr Virus ◽  
Nuclear Factor Kappa B ◽  
Latent Membrane Protein ◽  
Latent Membrane Protein 1 ◽  
Nuclear Factor ◽  
Barr Virus ◽  
Nuclear Factor Kappa ◽  
Epstein Barr

Epstein Barr virus-positive lymphoma results from the loss of homeostatic balance between Epstein Barr virus and immune cells. In this study, we investigated the mechanism underlying reduction in Epstein Barr virus-positive lymphoma cell proliferation and apoptosis by silymarin, an anti-inflammatory/antioxidant molecule extracted from Silybum�marianum (milk thistle). We examined the effect of silymarin on Raji cell proliferation, apoptosis, the expression of latent membrane protein�1, the proteins related to apoptosis, and the activation of nuclear factor kappa-B. Results showed that silymarin inhibited the proliferation and promoted apoptosis of Raji cells in a concentration-dependent manner. Also, silymarin reduced phosphorylated inhibitor of nuclear factor kappa-B and p65 levels. Silymarin treatment elevated latent membrane protein 1 expression and knockdown of this protein led to increased proliferation inhibition and apoptosis by silymarin. In conclusion, nuclear factor kappa-B and latent membrane protein 1 knockdown could work in concert with silymarin in suppressing Epstein Barr virus-positive lymphoma cell proliferation and inducing apoptosis.

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