Advances in melanoma senescence and potential clinical application

Pigment Cell Melanoma Res. 2011 Apr;24(2):295-308. doi: 10.1111/j.1755-148X.2010.00820.x. Epub 2011 Jan 11.

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.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Biomarkers / metabolism
  • Cell Cycle
  • Cell Proliferation
  • Cellular Senescence / physiology*
  • Chromosomal Proteins, Non-Histone / genetics
  • Chromosomal Proteins, Non-Histone / metabolism
  • Cyclin-Dependent Kinase Inhibitor p21 / genetics
  • Cyclin-Dependent Kinase Inhibitor p21 / metabolism
  • Humans
  • Intracellular Signaling Peptides and Proteins / genetics
  • Intracellular Signaling Peptides and Proteins / metabolism
  • Melanoma / pathology
  • Melanoma / physiopathology*
  • Microphthalmia-Associated Transcription Factor / genetics
  • Microphthalmia-Associated Transcription Factor / metabolism
  • Oncogene Proteins / genetics
  • Oncogene Proteins / metabolism
  • Oncogenes
  • Phenotype
  • Poly-ADP-Ribose Binding Proteins
  • Protein-Tyrosine Kinases / genetics
  • Protein-Tyrosine Kinases / metabolism
  • Proto-Oncogene Proteins c-myc / genetics
  • Proto-Oncogene Proteins c-myc / metabolism
  • Syk Kinase
  • T-Box Domain Proteins / genetics
  • T-Box Domain Proteins / metabolism
  • Tumor Suppressor Proteins / genetics
  • Tumor Suppressor Proteins / metabolism

Substances

  • Biomarkers
  • Chromosomal Proteins, Non-Histone
  • Cyclin-Dependent Kinase Inhibitor p21
  • DEK protein, human
  • Intracellular Signaling Peptides and Proteins
  • Microphthalmia-Associated Transcription Factor
  • Oncogene Proteins
  • Poly-ADP-Ribose Binding Proteins
  • Proto-Oncogene Proteins c-myc
  • T-Box Domain Protein 2
  • T-Box Domain Proteins
  • Tumor Suppressor Proteins
  • Protein-Tyrosine Kinases
  • SYK protein, human
  • Syk Kinase