title: Epigenetics and senescence: learning from the INK4-ARF locus.
abstract: 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.
authors.affiliation: Centre de Regulació Genómica, Universitat Pompeu Fabra, Barcelona, Spain.
authors.forename: Elisabeth
authors.initials: E
authors.lastname: Simboeck
authors.forename: Joana D
authors.initials: JD
authors.lastname: Ribeiro
authors.forename: Sophia
authors.initials: S
authors.lastname: Teichmann
authors.forename: Luciano
authors.initials: L
authors.lastname: Di Croce
mesh_terms: D000818:Animals; D016922:Cellular Senescence / Q000235:genetics* / Q000502:physiology*; D050756:Cyclin-Dependent Kinase Inhibitor Proteins / Q000235:genetics / Q000378:metabolism*; D044127:Epigenesis, Genetic; D005786:Gene Expression Regulation / Q000502:physiology*; D006801:Humans; D034882:Lamins / Q000378:metabolism
chemical_list: D050756:Cyclin-Dependent Kinase Inhibitor Proteins; D034882:Lamins