Variable expression of Epstein–Barr virus-induced gene 3 during normal B-cell differentiation and among B-cell lymphomas

2006 ◽  
Vol 209 (3) ◽  
pp. 360-368 ◽  
Author(s):  
F Larousserie ◽  
E Bardel ◽  
A Coulomb L'Herminé ◽  
D Canioni ◽  
N Brousse ◽  
...  
Cell ◽  
1982 ◽  
Vol 30 (2) ◽  
pp. 415-425 ◽  
Author(s):  
David A. Thorley-Lawson ◽  
Robert T. Schooley ◽  
Atul K. Bhan ◽  
Lee M. Nadler

2013 ◽  
Vol 13 (8) ◽  
pp. 2035-2043 ◽  
Author(s):  
S. Furukawa ◽  
L. Wei ◽  
S. M. Krams ◽  
C. O. Esquivel ◽  
O. M. Martinez

2018 ◽  
Vol 9 ◽  
Author(s):  
Pier P. Piccaluga ◽  
Alessandra Weber ◽  
Maria R. Ambrosio ◽  
Yonis Ahmed ◽  
Lorenzo Leoncini

2011 ◽  
Vol 18 (5) ◽  
pp. 349-355 ◽  
Author(s):  
Patrick Adam ◽  
Irina Bonzheim ◽  
Falko Fend ◽  
Leticia Quintanilla-Martínez

2010 ◽  
Vol 84 (22) ◽  
pp. 11670-11678 ◽  
Author(s):  
Sarah D. Linnstaedt ◽  
Eva Gottwein ◽  
Rebecca L. Skalsky ◽  
Micah A. Luftig ◽  
Bryan R. Cullen

ABSTRACT Infection of resting primary human B cells by Epstein-Barr virus (EBV) results in their transformation into indefinitely proliferating lymphoblastoid cell lines (LCLs). LCL formation serves as a model for lymphomagenesis, and LCLs are phenotypically similar to EBV-positive diffuse large B-cell lymphomas (DLBCLs), which represent a common AIDS-associated malignancy. B-cell infection by EBV induces the expression of several cellular microRNAs (miRNAs), most notably miR-155, which is overexpressed in many tumors and can induce B-cell lymphomas when overexpressed in animals. Here, we demonstrate that miR-155 is the most highly expressed miRNA in LCLs and that the selective inhibition of miR-155 function specifically inhibits the growth of both LCLs and the DLBCL cell line IBL-1. Cells lacking miR-155 are inefficient in progressing through S phase and spontaneously undergo apoptosis. In contrast, three other B-cell lymphoma lines, including two EBV-positive Burkitt's lymphoma cell lines, grew normally in the absence of miR-155 function. These data identify the induction of cellular miR-155 expression by EBV as critical for the growth of both laboratory-generated LCLs and naturally occurring DLBCLs and suggest that targeted inhibition of miR-155 function could represent a novel approach to the treatment of DLBCL in vivo.


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