title: Advances in melanoma senescence and potential clinical application.
abstract: Normal cells possess a limited proliferative life span, after which they enter a state of irreversible growth arrest, called replicative senescence, which acts as a potent barrier against transformation. Transformed cells have escaped the process of replicative senescence and theoretically can not re-enter senescence. However, recent observations showed that transformed cells, and particularly the melanoma cells, can still undergo oncogene or stress-induced senescence. This senescence state is accompanied by many of the markers associated with replicative senescence, such as flattened shape, increased acidic β-galactosidase activity, characteristic changes in gene expression and growth arrest. Interestingly, in some cancers, senescence induction following chemotherapy has been correlated with a favorable patient outcome. In this review, we gathered recent results describing senescence-like phenotype induction in melanoma cells and discuss why senescence may also be exploited as a therapeutic strategy in melanoma.
authors.affiliation: Inserm, U895, Equipe 1, Biologie et Pathologies des Mélanocytes: de la Pigmentation Cutanée au Mélanome, C3M, Nice, France.
authors.forename: Sandy
authors.initials: S
authors.lastname: Giuliano
authors.forename: Mickaël
authors.initials: M
authors.lastname: Ohanna
authors.forename: Robert
authors.initials: R
authors.lastname: Ballotti
authors.forename: Corine
authors.initials: C
authors.lastname: Bertolotto
mesh_terms: D015415:Biomarkers / Q000378:metabolism; D002453:Cell Cycle; D049109:Cell Proliferation; D016922:Cellular Senescence / Q000502:physiology*; D002868:Chromosomal Proteins, Non-Histone / Q000235:genetics / Q000378:metabolism; D050759:Cyclin-Dependent Kinase Inhibitor p21 / Q000235:genetics / Q000378:metabolism; D006801:Humans; D047908:Intracellular Signaling Peptides and Proteins / Q000235:genetics / Q000378:metabolism; D008545:Melanoma / Q000473:pathology / Q000503:physiopathology*; D051739:Microphthalmia-Associated Transcription Factor / Q000235:genetics / Q000378:metabolism; D015513:Oncogene Proteins / Q000235:genetics / Q000378:metabolism; D009857:Oncogenes; D010641:Phenotype; D000075223:Poly-ADP-Ribose Binding Proteins; D011505:Protein-Tyrosine Kinases / Q000235:genetics / Q000378:metabolism; D016271:Proto-Oncogene Proteins c-myc / Q000235:genetics / Q000378:metabolism; D000072377:Syk Kinase; D020825:T-Box Domain Proteins / Q000235:genetics / Q000378:metabolism; D025521:Tumor Suppressor Proteins / Q000235:genetics / Q000378:metabolism
chemical_list: D015415:Biomarkers; D002868:Chromosomal Proteins, Non-Histone; D050759:Cyclin-Dependent Kinase Inhibitor p21; C084738:DEK protein, human; D047908:Intracellular Signaling Peptides and Proteins; D051739:Microphthalmia-Associated Transcription Factor; D015513:Oncogene Proteins; D000075223:Poly-ADP-Ribose Binding Proteins; D016271:Proto-Oncogene Proteins c-myc; C097348:T-Box Domain Protein 2; D020825:T-Box Domain Proteins; D025521:Tumor Suppressor Proteins; D011505:Protein-Tyrosine Kinases; C000606896:SYK protein, human; D000072377:Syk Kinase