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Stress-activated protein kinases-tumor suppressors or tumor initiators?

机译:应激激活的蛋白激酶-抑癌剂还是肿瘤引发剂?

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The biology and the pathology of the stress-activated protein kinases (SAPKs; p38s and c-Jun-NH(2)-terminal kinases (JNKs)) are somewhat confusing. In some systems, these enzymes augment cell proliferation whereas in other cells they support growth arrest and tumor suppressing activity. Similarly, in some types of cancer SAPKs' activity is suppressed while in others SAPKs seem to be an essential part of the transformative machinery. Revealing the role of SAPKs in cancer is important for planning an appropriate therapeutic strategy. Here, I describe the data supporting the role of SAPKs as tumor suppressors in some systems and as pro-oncogenic in others. Possible resolutions for the paradox of stress kinases are also discussed.
机译:应力激活蛋白激酶(SAPKs; p38s和c-Jun-NH(2)-末端激酶(JNKs))的生物学和病理学有些令人困惑。在某些系统中,这些酶增强细胞增殖,而在其他细胞中,它们则支持生长停滞和肿瘤抑制活性。同样,在某些类型的癌症中,SAPKs的活性受到抑制,而在另一些类型中,SAPKs似乎是转化机制的重要组成部分。揭示SAPK在癌症中的作用对于规划适当的治疗策略很重要。在这里,我描述了支持SAPK在某些系统中起抑癌作用而在另一些系统中起促癌作用的数据。还讨论了应激激酶悖论的可能解决方案。

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