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ROCK 和 MRCK 激酶在癌细胞迁移可塑性中的调节作用。

The regulatory roles of ROCK and MRCK kinases in the plasticity of cancer cell migration.

机构信息

Department of Pharmacology, Penn State Hershey College of Medicine, Hershey, PA 17033, USA.

Department of Pharmacology, Penn State Hershey College of Medicine, Hershey, PA 17033, USA.

出版信息

Cancer Lett. 2015 Jun 1;361(2):185-96. doi: 10.1016/j.canlet.2015.03.017. Epub 2015 Mar 18.

Abstract

Metastatic cancer cells show great plasticity in their migratory mechanisms. In this review we briefly describe the signal transduction pathways associated with the ROCK and MRCK kinases and their roles in cancer cell migration and in its plasticity. With respect to therapeutic strategies targeting metastatic cancers, selectively blocking a single target, such as ROCK or MRCK, can induce alternate modes of cancer cell migration (i.e. plasticity) making the treatment ineffective. To address the problem of plasticity, we will discuss the strategy of simultaneous targeting of both ROCK and MRCK as an effective anti-metastatic therapeutics.

摘要

转移性癌细胞在其迁移机制中表现出很强的可塑性。在这篇综述中,我们简要描述了与 ROCK 和 MRCK 激酶相关的信号转导通路及其在癌细胞迁移及其可塑性中的作用。关于针对转移性癌症的治疗策略,选择性地阻断单个靶点,如 ROCK 或 MRCK,可能会诱导癌细胞迁移的替代模式(即可塑性),从而使治疗无效。为了解决可塑性问题,我们将讨论同时靶向 ROCK 和 MRCK 的策略,作为一种有效的抗转移治疗方法。

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