RSK in tumorigenesis: Connections to steroid signaling

被引:49
作者
Eisinger-Mathason, T. S. Karin [1 ,2 ]
Andrade, Josefa [1 ,2 ]
Lannigan, Deborah A. [1 ,2 ]
机构
[1] Univ Virginia, Dept Microbiol, Charlottesville, VA 22908 USA
[2] Univ Virginia, Ctr Cell Signaling, Charlottesville, VA 22908 USA
关键词
MAPK pathway; p90 ribosomal S6 kinase; Estrogen receptor; Androgen receptor; Tumorigenesis; RIBOSOMAL S6 KINASE; ACTIVATED PROTEIN-KINASE; EPIDERMAL-GROWTH-FACTOR; BREAST-CANCER CELLS; BOX BINDING PROTEIN-1; C-FOS PROTOONCOGENE; ESTROGEN-RECEPTOR EXPRESSION; X-LINKED GENES; LUNG-CANCER; ANDROGEN RECEPTOR;
D O I
10.1016/j.steroids.2009.12.010
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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. (C) 2009 Elsevier Inc. All rights reserved.
引用
收藏
页码:191 / 202
页数:12
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