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Cancer Biol Ther. 2012 Sep;13(11):992-1000. doi: 10.4161/cbt.21116. Epub 2012 Jul 24.

Regulation of oncogene-induced cell cycle exit and senescence by chromatin modifiers.

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1
Department of Pharmacology and NYU Cancer Institute, NYU Langone Medical Center, New York, NY, USA. gregory.david@nyumc.org

Abstract

Oncogene activation leads to dramatic changes in numerous biological pathways controlling cellular division, and results in the initiation of a transcriptional program that promotes transformation. Conversely, it also triggers an irreversible cell cycle exit called cellular senescence, which allows the organism to counteract the potentially detrimental uncontrolled proliferation of damaged cells. Therefore, a tight transcriptional control is required at the onset of oncogenic signal, coordinating both positive and negative regulation of gene expression. Not surprisingly, numerous chromatin modifiers contribute to the cellular response to oncogenic stress. While these chromatin modifiers were initially thought of as mere mediators of the cellular response to oncogenic stress, recent studies have uncovered a direct and specific regulation of chromatin modifiers by oncogenic signals. We review here the diverse functions of chromatin modifiers in the cellular response to oncogenic stress, and discuss the implications of these findings on the regulation of cell cycle progression and proliferation by activated oncogenes.

PMID:
22825329
PMCID:
PMC3461821
DOI:
10.4161/cbt.21116
[Indexed for MEDLINE]
Free PMC Article
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