期刊
CELL CYCLE
卷 11, 期 1, 页码 57-64出版社
TAYLOR & FRANCIS INC
DOI: 10.4161/cc.11.1.18775
关键词
cell cycle; cyclin E; Cdk2; Fbw7; E2F; p21; p27; regulatory network
类别
资金
- Chicago Biomedical Consortium
- Chicago Community Trust
- NIH [R01HL098608]
- Sidney Kimmel Foundation
Cancers of diverse cell lineages express high levels of cyclin E, and in various studies, cyclin E overexpression correlates with increased tumor aggression. One way that normal control of cyclin E expression is disabled in cancer cells is via loss-of-function mutations sustained by FBXW7. This gene encodes the Fbw7 tumor suppressor protein that provides substrate specificity for a ubiquitin ligase complex that targets multiple oncoproteins for degradation. Numerous other mechanisms besides Fbw7 mutations can deregulate cyclin E expression and activity in cancer cells. Recent reports demonstrate that inappropriate cyclin E expression may have far-reaching biological consequences for cell physiology, including altering gene expression programs governing proliferation, differentiation, survival and senescence. In this Perspective, we discuss the function of mammalian cyclin E in the context of these new data as well as the complex network that connects cyclin E functions to the cellular controls regulating its expression and activity.
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