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Stop and go - Anti-proliferative and mitogenic functions of the transcription factor C/EBP beta

  1. Author:
    Sebastian, T.
    Johnson, P. F.

  2. Author Address

    NCI, Lab Prot Dynam & Signaling, Frederick, MD 21702 USA.;Johnson, PF, NCI, Lab Prot Dynam & Signaling, Bldg 539,Rm 122, Frederick, MD 21702 USA.;johnsopf@ncifcrf.gov
    1. Year: 2006
    2. Date: May
  2. Journal: Cell Cycle
    1. 5
    2. 9
    3. Pages: 953-957
  4. Type of Article: Article
  5. ISSN: 1538-4101
  1. Abstract:

    Oncogene-induced senescence (OIS) is an irreversible form of cell cycle arrest that can be elicited by overexpression of oncogenes such as Ras(V12) 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/EBP beta, a downstream target of Ras signaling, is an essential component of Ras(V12)-mediated senescence in mouse embryo fibroblasts (MEFs). C/EBP beta induces cell cycle arrest through a mechanism requiring RB:E2F repressor complexes and negatively regulates several E2F target genes. Although C/EBP beta has tumor suppressor-like activity in MEFs, other observations point to critical pro-oncogenic functions for C/EBP beta in certain cancers. Here we review the evidence for positive and negative cell cycle regulation by C/EBP beta and discuss possible mechanisms by which this transcription factor could participate in both cellular senescence and oncogenic transformation.

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External Sources

  1. View record in Web of Science®
  2. WOS: 000238575200011

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