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Blood, 15 August 2005, Vol. 106, No. 4, pp. 1382-1391.
Prepublished online as a Blood First Edition Paper on May 12, 2005; DOI 10.1182/blood-2004-10-3819.
 Previous Article | Next Article 
Submitted October 1, 2004
Accepted April 20, 2005
c-Jun N-terminal kinase (JNK) is required for survival and proliferation of B lymphoma cells
Murali Gururajan, Roger Chui, Anbu K Karuppannan, Jiyuan Ke, C D Jennings, and Subbarao Bondada*
Graduate Center for Toxicology, University of Kentucky, Lexington, KY, USA; Department of Microbiology, Immunology & Molecular Genetics, University of Kentucky, Lexington, KY, USA
Department of Microbiology, Immunology & Molecular Genetics, University of Kentucky, Lexington, KY, USA
Department of Pathology & Laboratory Medicine, University of Kentucky, Lexington, KY, USA
Department of Microbiology, Immunology & Molecular Genetics, University of Kentucky, Lexington, KY, USA; Sanders Brown Center on Aging, University of Kentucky, Lexington, KY, USA; Graduate Center for Toxicology, University of Kentucky, Lexington, KY, USA
* Corresponding author; email: bondada{at}uky.edu.
Several primary murine and human B lymphomas and cell lines were found to constitutively express high levels of activated form of c-jun N-terminal kinase (JNK), a member of the MAP kinase family. Proliferation of murine B lymphomas CH31, CH12.Lx, BKS-2, WEHI-231, and the human B lymphomas BJAB, RAMOS, RAJI, OCI-Ly7 and OCI-Ly10 was strongly inhibited by SP600125, an anthrapyrazolone inhibitor of JNK, in a dose dependent manner. The lymphoma cells underwent apoptosis and arrested at G2/M phase of cell cycle. Furthermore, JNK specific small interfering RNA (RNAi) inhibited the growth of both murine and human B lymphomas. Thus in the B-lymphoma model JNK appears to have a unique prosurvival role. Survival signals provided by CD40 and IL-10 together reversed the growth inhibition induced by the JNK inhibitor. c-Myc protein levels were reduced in the presence of both SP600125 and JNK specific siRNA and CD40 ligation restored c-Myc levels. Moreover, Bcl-xL rescued WEHI-231 cells from apoptosis induced by the JNK inhibitor. JNK inhibitor also reduced levels of Egr-1 protein and over-expressing Egr-1 partially rescued lymphoma cells from apoptosis. Thus JNK may act via c-Myc and Egr-1, which were shown to be important for B lymphoma survival and growth.
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