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Cell Cycle. 2012 Jan 1;11(1):57-64. doi: 10.4161/cc.11.1.18775. Epub 2012 Jan 1.

An integrated view of cyclin E function and regulation.

Author information

1
Department of Medicine, Hematology/Oncology Division, Integrated Graduate Program in the Life Sciences, Northwestern University Feinberg School of Medicine, Chicago, IL, USA.

Abstract

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 review, 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.

PMID:
22186781
PMCID:
PMC3272232
DOI:
10.4161/cc.11.1.18775
[Indexed for MEDLINE]
Free PMC Article

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