c-Jun N-terminal kinase (JNK) is required for survival and proliferation of B-lymphoma cells
作者： Murali Gururajan , Roger Chui , Anbu K. Karuppannan , Jiyuan Ke , C. Darrell Jennings
DOI: 10.1182/BLOOD-2004-10-3819
关键词:
摘要: Several primary murine and human B lymphomas cell lines were found to constitutively express high levels of the activated form c-jun N-terminal kinase (JNK), a member mitogen-activated protein (MAP) family. Proliferation CH31, CH12.Lx, BKS-2, WEHI-231 BJAB, RAMOS, RAJI, OCI-Ly7, OCI-Ly10 was strongly inhibited by SP600125, an anthrapyrazolone inhibitor JNK, in dose-dependent manner. The lymphoma cells underwent apoptosis arrested at G2/M phase cycle. Furthermore, JNK-specific small interfering RNA (siRNA) growth both lymphomas. Thus B-lymphoma model, JNK appears have unique prosurvival role. Survival signals provided CD40 interleukin-10 (IL-10) together reversed inhibition induced inhibitor. c-Myc reduced presence SP600125 siRNA, ligation restored levels. Moreover, Bcl-xL rescued from also early response gene-1 (Egr-1) protein, overexpressing Egr-1 partially apoptosis. Thus, may act via Egr-1, which shown be important for survival growth. (Blood. 2005;106:1382-1391)
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