Heasley Lynn E, Han Sun-Young
Department of Medicine, University of Colorado Health Sciences Center, Denver, CO 80262, USA.
Mol Cells. 2006 Apr 30;21(2):167-73.
The literature provides strong precedent for both pro-tumorigenic and tumor suppressor roles for the c-Jun N-terminal kinases (JNKs) in the setting of oncogenesis. Clearly, JNKs are activated by numerous oncogenes and growth factors and the literature documents a role for these MAP kinases in cell proliferation and transformation. By contrast, JNKs mediate signals from diverse stimuli that result in cell death or differentiation and a role for JNKs as tumor suppressors has emerged. This enigmatic nature of the JNKs in the setting of oncogenesis is considered herein. Further illumination of the complex and context-dependent functions of the JNKs in cancer cells is of obvious importance for the rational use of small molecule JNK inhibitors as therapeutics.
文献为c-Jun氨基末端激酶（JNKs）在肿瘤发生过程中促肿瘤和肿瘤抑制作用均提供了有力的先例。显然，JNKs可被多种癌基因和生长因子激活，并且文献记载了这些丝裂原活化蛋白激酶在细胞增殖和转化中的作用。相比之下，JNKs介导来自多种刺激的信号，这些信号导致细胞死亡或分化，并且JNKs作为肿瘤抑制因子的作用已显现出来。本文将探讨JNKs在肿瘤发生过程中的这种神秘特性。进一步阐明JNKs在癌细胞中复杂且依赖于背景的功能对于合理使用小分子JNK抑制剂作为治疗手段显然具有重要意义。
