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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. This Article Full Text Full Text (PDF) All Versions of this Article: 2004-10-3819v1 106/4/1382    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Gururajan, M. Articles by Bondada, S. Search for Related Content PubMed PubMed Citation Articles by Gururajan, M. Articles by Bondada, S. Related Collections Neoplasia Signal Transduction Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  NEOPLASIA 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. Darrell Jennings, and Subbarao Bondada From the Department of Microbiology, Immunology, & Molecular Genetics, the Sanders Brown Center on Aging, the Graduate Center for Toxicology, and the Department of Pathology & Laboratory Medicine, University of Kentucky, Lexington, KY. Several primary murine and human B lymphomas and cell lines were found to constitutively express high levels of the activated form of c-jun N-terminal kinase (JNK), a member of the mitogen-activated protein (MAP) kinase family. Proliferation of murine B lymphomas CH31, CH12.Lx, BKS-2, and 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 the G2/M phase of cell cycle. Furthermore, JNK-specific small interfering RNA (siRNA) 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 interleukin-10 (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. The JNK inhibitor also reduced levels of early growth response gene-1 (Egr-1) protein, and overexpressing 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. (Blood. 2005;106:1382-1391) CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: J. S. Chang, T. Wendt, W. Qu, L. Kong, Y. S. Zou, A. M. Schmidt, and S.-F. Yan Oxygen Deprivation Triggers Upregulation of Early Growth Response-1 by the Receptor for Advanced Glycation End Products Circ. Res., April 25, 2008; 102(8): 905 - 913. [Abstract] [Full Text] [PDF] R. Rouget, Y. Auclair, M. Loignon, E. B. Affar, and E. A. Drobetsky A Sensitive Flow Cytometry-based Nucleotide Excision Repair Assay Unexpectedly Reveals That Mitogen-activated Protein Kinase Signaling Does Not Regulate the Removal of UV-induced DNA Damage in Human Cells J. Biol. 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