RSK in tumorigenesis: connections to steroid signaling.
RSK in tumorigenesis: connections to steroid signaling.
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DOI：
10.1016/j.steroids.2009.12.010
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发表时间：
2010-03
期刊：
影响因子：
2.7
通讯作者：
Lannigan, Deborah A.
中科院分区：
文献类型：
--
作者：
Eisinger-Mathason, T. S. Karin;Andrade, Josefa;Lannigan, Deborah A.
丝氨酸/苏氨酸蛋白激酶家族RSK与多种激素依赖型和非激素依赖型癌症有关。然而，很少有人考虑RSK作为类固醇激素非基因组效应的下游介质或它们促进类固醇受体介导的基因表达的能力。类固醇激素信号转导可以直接激活MEK/ERK/RSK通路，调节转化细胞的增殖和存活。到目前为止，RSK和类固醇激素受体介导的增殖/存活的多种机制已经阐明。例如，RSK通过控制雌激素受体共激活物细胞周期蛋白D1的水平来促进乳腺和前列腺癌细胞的增殖。而在肺和其他肿瘤中，RSK可能通过雌激素介导的线粒体完整性调节来控制细胞凋亡。因此，RSKs可能是许多不同转化组织中重要的抗癌治疗靶点。最近发现的RSK特异性抑制剂将促进我们目前对RSK转化过程的理解，并推动这些研究进入动物和临床模型。在这篇综述中，我们探讨了RSK在肿瘤发生中的相关机制，以及它们与类固醇激素信号的关系。
The Ser/Thr kinase family, RSK, has been implicated in numerous types of hormone-dependent and -independent cancers. However, there has been little consideration of RSKs as downstream mediators of steroid hormone non-genomic effects or of their ability to facilitate steroid receptor-mediated gene expression. Steroid hormone signaling can directly stimulate the MEK/ERK/RSK pathway to regulate cellular proliferation and survival in transformed cells. To date, multiple mechanisms of RSK and steroid hormone receptor-mediated proliferation/survival have been elucidated. For example, RSK enhances proliferation of breast and prostate cancer cells via its ability to control the levels of the estrogen receptor co-activator, cyclin D1. While in lung and other tumors RSK may control apoptosis via estrogen-mediated regulation of mitochondrial integrity. Thus the RSKs could be important anti-cancer therapeutic targets in many different transformed tissues. The recent discovery of RSK-specific inhibitors will advance our current understanding of RSK in transformation and drive these studies into animal and clinical models. In this review we explore the mechanisms associated with RSK in tumorigenesis and their relationship to steroid hormone signaling.
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