Wagner Erwin F, Nebreda Angel R
Centro Nacional de Investigaciones Oncológicas, C/Melchor Fernández Almagro 3, Madrid 28029, Spain.
Nat Rev Cancer. 2009 Aug;9(8):537-49. doi: 10.1038/nrc2694.
Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (MAPK) family members function in a cell context-specific and cell type-specific manner to integrate signals that affect proliferation, differentiation, survival and migration. Consistent with the importance of these events in tumorigenesis, JNK and p38 MAPK signalling is associated with cancers in humans and mice. Studies in mouse models have been essential to better understand how these MAPKs control cancer development, and these models are expected to provide new strategies for the design of improved therapeutic approaches. In this Review we highlight the recent progress made in defining the functions of the JNK and p38 MAPK pathways in different cancers.
Jun氨基末端激酶(JNK)和p38丝裂原活化蛋白激酶(MAPK)家族成员以细胞背景特异性和细胞类型特异性的方式发挥作用,整合影响细胞增殖、分化、存活和迁移的信号。鉴于这些事件在肿瘤发生中的重要性,JNK和p38 MAPK信号传导与人类和小鼠的癌症相关。对小鼠模型的研究对于更好地理解这些MAPK如何控制癌症发展至关重要,并且这些模型有望为设计改进的治疗方法提供新策略。在本综述中,我们重点介绍了在确定JNK和p38 MAPK通路在不同癌症中的功能方面取得的最新进展。