Abstract
Cellular senescence is an irreversible arrest of proliferation. It is activated when a cell encounters stress such as DNA damage, telomere shortening or oncogene activation. Like apoptosis, it impedes tumour progression and acts as a barrier that pre-neoplastic cells must overcome during their evolution toward the full tumourigenic state. This review focuses on the role of transcriptional regulators in the control of cellular senescence, explores how their function is perturbed in cancer and discusses the potential to harness this knowledge for future cancer therapies.
Publication types
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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ADP-Ribosylation Factors / genetics
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ADP-Ribosylation Factors / metabolism
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ADP-Ribosylation Factors / physiology
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Animals
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Apoptosis / genetics
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Apoptosis / physiology
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Cellular Senescence / genetics*
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Cyclin-Dependent Kinase Inhibitor p16 / genetics
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Cyclin-Dependent Kinase Inhibitor p16 / metabolism
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Cyclin-Dependent Kinase Inhibitor p16 / physiology
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Gene Expression Regulation / physiology*
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Genetic Loci / genetics
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Genetic Loci / physiology
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Humans
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Models, Biological
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Signal Transduction / genetics
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Signal Transduction / physiology
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Transcription, Genetic / physiology
Substances
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Cyclin-Dependent Kinase Inhibitor p16
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ADP-Ribosylation Factors