The roles of latent membrane protein 1 of Epstein-Barr virus in cell growth, proliferation and survival in a rat fibroblast cell line

1999 ◽  
Author(s):  
Pui-yue Li
1994 ◽  
Vol 24 (6) ◽  
pp. 1467-1470 ◽  
Author(s):  
Qin Zhang ◽  
Louise Brooks ◽  
Pierre Busson ◽  
Fred Wang ◽  
Dominique Charron ◽  
...  

Virology ◽  
2011 ◽  
Vol 413 (1) ◽  
pp. 19-25 ◽  
Author(s):  
Chun-Wei Lee ◽  
Shr-Jeng Jim Leu ◽  
Ruei-Ying Tzeng ◽  
Sheng–Fan Wang ◽  
Shu-Chun Tsai ◽  
...  

2006 ◽  
Vol 80 (16) ◽  
pp. 8038-8046 ◽  
Author(s):  
Jyotsna Pandya ◽  
Dennis M. Walling

ABSTRACT The Epstein-Barr virus (EBV) is an oncogenic human herpesvirus. EBV latent membrane protein 1 (LMP-1) is a viral oncogene that manifests its oncogenic phenotype through activation of cellular signaling pathways involved in cell growth, survival, differentiation, and transformation. Lytic LMP-1 (lyLMP-1) is a related EBV gene without oncogenic properties. The lyLMP-1 gene is found in 60% of the EBV strains circulating in nature, but it is not found in EBV strains associated with nasopharyngeal carcinoma. We recently demonstrated that lyLMP-1 down-regulates the half-life of LMP-1 in epithelial cells. Therefore in this study, we tested the hypothesis that lyLMP-1 concomitantly down-regulates LMP-1 oncogenic activity. The results demonstrated that lyLMP-1 inhibits LMP-1-mediated intracellular signaling activation, epithelial cell growth and survival, and fibroblast cell transformation in a dose-dependent manner. Lytic LMP-1 manifested this effect through the promotion of LMP-1 degradation and a reduction in the expressed quantity of LMP-1. Thus, lyLMP-1 functions as a posttranslational negative regulator of LMP-1 oncogenesis. These results support a model of EBV-associated epithelial oncogenesis in which lyLMP-1 may act in vivo to reduce the risk of LMP-1-mediated transformation and is therefore subjected to negative selection in nasopharyngeal carcinoma pathogenesis.


2007 ◽  
Vol 81 (17) ◽  
pp. 9299-9306 ◽  
Author(s):  
Makoto Fukuda ◽  
Richard Longnecker

ABSTRACT Epstein-Barr virus (EBV) latent membrane protein 2A (LMP2A) is widely expressed in EBV-infected cells within the infected human host and EBV-associated malignancies, suggesting that LMP2A is important for EBV latency, persistence, and EBV-associated tumorigenesis. Previously, we demonstrated that LMP2A provides an antiapoptotic signal through the activation of phosphatidylinositol 3-kinase (PI3-K)/Akt pathway in vitro. However, the exact function of LMP2A in tumor progression is not well understood. In this study, we found that LMP2A did not induce anchorage-independent cell growth in a human keratinocyte cell line, HaCaT, but did in a human gastric carcinoma cell line, HSC-39. In addition, LMP2A activated the PI3-K/Akt pathway in both HaCaT and HSC-39 cells; however, LMP2A did not activate Ras in HaCaT cells but did in HSC-39 cells. Furthermore, the Ras inhibitors manumycin A and a dominant-negative form of Ras (RasN17) and the PI3-K inhibitor LY294002 blocked LMP2A-mediated Akt phosphorylation and anchorage-independent cell growth in HSC-39 cells. These results suggest that constitutive activation of the Ras/PI3-K/Akt pathway by LMP2A is a key factor for LMP2A-mediated transformation.


Intervirology ◽  
2021 ◽  
Vol 64 (2) ◽  
pp. 69-80
Author(s):  
Hai-Yu Wang ◽  
Lingling Sun ◽  
Ping Li ◽  
Wen Liu ◽  
Zhong-Guang Zhang ◽  
...  

<b><i>Objective:</i></b> To investigate the relationship between hematologic tumors and Epstein-Barr virus (EBV)-encoded small noncoding RNA (EBER) variations as well as latent membrane protein 1 (LMP1) variations. <b><i>Methods:</i></b> Patients with leukemia and myelodysplastic syndrome (MDS) were selected as subjects. Genotypes 1/2 and genotypes F/f were analyzed using the nested PCR technology, while EBER and LMP1 subtypes were analyzed by the nested PCR and DNA sequencing. <b><i>Results:</i></b> Type 1 was more dominant than type 2, found in 59 out of 82 (72%) leukemia and in 31 out of 35 (88.6%) MDS, while type F was more prevalent than type f in leukemia (83/85, 97.6%) and MDS (29/31, 93.5%) samples. The distribution of EBV genotypes 1/2 was not significantly different among leukemia, MDS, and healthy donor groups, neither was that of EBV genotypes F/f. EB-6m prototype was the dominant subtype of EBER in leukemia and MDS (73.2% [30/41] and 83.3% [10/12], respectively). The frequency of EB-6m was lower than that of healthy people (96.7%, 89/92), and the difference was significant (<i>p</i> &#x3c; 0.05). China 1 subtype was the dominant subtype of LMP1 in leukemia and MDS (70% [28/40] and 90% [9/10], respectively), and there was no significant difference in the distribution of LMP1 subtypes among the 3 groups (<i>p</i> &#x3e; 0.05). <b><i>Conclusion:</i></b> The distribution of EBV 1/2, F/f, EBER, and LMP1 subtypes in leukemia and MDS was similar to that in the background population in Northern China, which means that these subtypes may be rather region-restricted but not associated with leukemia and MDS pathogenesis.


Cancer ◽  
2010 ◽  
Vol 116 (4) ◽  
pp. 880-887 ◽  
Author(s):  
Jeffrey J. Tarrand ◽  
Michael J. Keating ◽  
Apostolia M. Tsimberidou ◽  
Susan O'Brien ◽  
Rocco P. LaSala ◽  
...  

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