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First published online June 8, 2005
doi: 10.1242/10.1242/jcs.02459

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Molecular stop signs: regulation of cell-cycle arrest by C/EBP transcription factors

Laboratory of Protein Dynamics and Signaling, Center for Cancer Research, NCI-Frederick, Frederick, MD 21702-1201, USA

e-mail: johnsopf{at}ncifcrf.gov

The CCAAT/enhancer-binding protein (C/EBP) family of transcription factors plays an important role in controlling cell proliferation and differentiation. C/EBP is a particularly potent regulator of cell-cycle exit and is induced in terminally differentiating adipocytes and myeloid cells, where it also activates differentiation-specific genes. The growth-inhibiting activity of C/EBP suppresses tumorigenesis in myeloid cells and possibly other tissues. In addition, recent work has identified C/EBP as a component of the p53-regulated growth arrest response elicited by DNA damage in epidermal keratinocytes. Several studies have explored the mechanism by which C/EBP blocks cell-cycle progression at the G1-S boundary, and several models have been proposed but no universally accepted mechanism has emerged. Controversial issues include whether C/EBP acts through an `off-DNA' mechanism to inhibit cyclin-dependent kinases, and whether and how it functions with the RB-E2F system to repress transcription of S-phase genes. Other C/EBP-family members have also been implicated in positive and negative control of cell proliferation, and the mechanisms underlying their growth-regulatory activities are beginning to be elucidated.

Key words: C/EBP, Cell cycle, Proliferation arrest

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