SASPense and DDRama in cancer and ageing

Nat Cell Biol. 2009 Aug;11(8):921-3. doi: 10.1038/ncb0809-921.

Abstract

Senescent cells alter their microenvironment by secreting a growing collection of factors, a phenomenon termed the senescence-associated secretory phenotype (SASP). Cellular senescence is often the result of nuclear DNA damage fuelling a chronic DNA damage response (DDR). Upstream elements of the DDR cascade are necessary for full blown SASP, and additional crosstalk occurs between the DDR and cytokine secretion.

Publication types

  • News
  • Comment

MeSH terms

  • Ataxia Telangiectasia Mutated Proteins
  • Cell Cycle Proteins / genetics
  • Cell Cycle Proteins / metabolism
  • Cells, Cultured
  • Cellular Senescence / physiology*
  • Checkpoint Kinase 2
  • Cytokines / metabolism*
  • DNA Damage*
  • DNA-Binding Proteins / genetics
  • DNA-Binding Proteins / metabolism
  • Fibroblasts / cytology
  • Fibroblasts / metabolism
  • Fibroblasts / radiation effects
  • Humans
  • Interleukin-6 / metabolism
  • Male
  • Models, Biological
  • Nuclear Proteins / genetics
  • Nuclear Proteins / metabolism
  • Protein Serine-Threonine Kinases / genetics
  • Protein Serine-Threonine Kinases / metabolism
  • RNA, Small Interfering / genetics
  • Signal Transduction / physiology*
  • Transfection
  • Tumor Suppressor Proteins / genetics
  • Tumor Suppressor Proteins / metabolism

Substances

  • Cell Cycle Proteins
  • Cytokines
  • DNA-Binding Proteins
  • Interleukin-6
  • NBN protein, human
  • Nuclear Proteins
  • RNA, Small Interfering
  • Tumor Suppressor Proteins
  • Checkpoint Kinase 2
  • ATM protein, human
  • Ataxia Telangiectasia Mutated Proteins
  • CHEK2 protein, human
  • Protein Serine-Threonine Kinases