Journal
BIOCHEMICAL PHARMACOLOGY
Volume 82, Issue 10, Pages 1361-1370Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.bcp.2011.07.084
Keywords
Transcription; Gene regulation; Epigenetics; Senescence; Polycomb
Categories
Funding
- Spanish Ministerio de Educacion y Ciencia
- AIRC [10-0177]
- AGAUR
- Foundation for Science and Technology (FCT) Portugal [SFRH/BD/15908/2005]
- Fundação para a Ciência e a Tecnologia [SFRH/BD/15908/2005] Funding Source: FCT
- ICREA Funding Source: Custom
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Cellular senescence is the biological consequence of aging. However, the same mechanisms that provoke senescence during aging have been proven to act in tumor suppression and thus to occur in premalignant cells. All the diverse aspects of the senescent phenotype, as are observed for many other cell fates, arise from alterations of the chromatin architecture. Relatively little is known overall about the changes in chromatin structure, and which regulatory networks are implicated in these. Major insight into the epigenetic contributions to senescence has been gained by studying the regulation of the INK4-ARF locus. Activation of the tumor suppressors encoded by this locus leads to an irreversible cell cycle exit. Importantly, epigenetic alterations at this locus have been associated with the onset of cancer. Here we discuss the recent findings that link epigenetics to the senescence pathway. (C) 2011 Elsevier Inc. All rights reserved.
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