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Perspectives
Stop and Go: Anti-Proliferative and Mitogenic Functions of the Transcription Factor C/EBPβ
Thomas Sebastian and Peter F. Johnson
volume 5 | issue 9
1 may 2006Pages: 953 - 957
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Oncogene-induced senescence (OIS) is an irreversible form of cell cycle arrest that can be elicited by over-expression of oncogenes such as RasV12 and requires activation of the Arf-p53 and RB tumor suppressor pathways. Increasing evidence implicates senescence as a bona fide tumor suppression mechanism in vivo. We recently discovered that the bZIP transcription factor C/EBPβ, a downstream target of Ras signaling, is an essential component of RasV12-mediated senescence in mouse embryo fibroblasts (MEFs). C/EBPβ induces cell cycle arrest through a mechanism requiring RB:E2F repressor complexes and negatively regulates several E2F target genes. Although C/EBPβ has tumor suppressor-like activity in MEFs, other observations point to critical pro-oncogenic functions for C/EBPβ in certain cancers. Here we review the evidence for positive and negative cell cycle regulation by C/EBPβ and discuss possible mechanisms by which this transcription factor could participate in both cellular senescence and oncogenic transformation.
We now provide open access to journal articles published online for one year or more. This article may be downloaded at the following link:
Download PDF If the document does not open, please right-click on the link (control-click on a Macintosh) and select the option to save the file to disk.