Chen Nanyue, She Qing-Bai, Bode Ann M, Dong Zigang
The Hormel Institute, University of Minnesota, Austin, Minnesota 55912.
Cancer Res. 2002 Mar 1;62(5):1300-4.
c-Jun NH(2)-terminal kinase (JNK) 1 and JNK2 have been assumed to complement each other and mediate the same or similar biological functions. However, our recent reports indicated that 7,12-dimethylbenz(a)anthracene/12-O-tetradecanoylphorbol-13-acetate-induced tumor development is suppressed in Jnk2 knockout mice but enhanced in Jnk1 knockout mice. In the present work, primary embryo cells were isolated from wild-type, Jnk1(-/-) and Jnk2(-/-) mice and used for cDNA microarray analysis. The patterns of gene expression in Jnk1(-/-), Jnk2(-/-), and wild-type cells are different. After 12-O-tetradecanoylphorbol-13-acetate treatment, the changes in the gene expression profiles in three different kinds of cells appear to agree with the differences in susceptibility to tumorigenesis of each respective animal model. These results suggest that JNK1 and JNK2 proteins have different roles in modulating cell function.
c-Jun氨基末端激酶(JNK)1和JNK2被认为相互补充并介导相同或相似的生物学功能。然而,我们最近的报告表明,在Jnk2基因敲除小鼠中,7,12-二甲基苯并(a)蒽/12-O-十四烷酰佛波醇-13-乙酸酯诱导的肿瘤发展受到抑制,而在Jnk1基因敲除小鼠中则增强。在本研究中,从野生型、Jnk1(-/-)和Jnk2(-/-)小鼠中分离出原代胚胎细胞,并用于cDNA微阵列分析。Jnk1(-/-)、Jnk2(-/-)和野生型细胞中的基因表达模式不同。用12-O-十四烷酰佛波醇-13-乙酸酯处理后,三种不同类型细胞中基因表达谱的变化似乎与各自动物模型对肿瘤发生的易感性差异一致。这些结果表明,JNK1和JNK2蛋白在调节细胞功能中具有不同的作用。