Stop and Go: Anti-Proliferative and Mitogenic Functions of the Transcription Factor C/EBPβ

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Abstract
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.

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