In Cellular Senescence, the Third Circle of the Cell Life's Network, p53 Acts Vital Role

Abstract

The cells rotationally live as Gap 1 (G1), DNA (deoxyribonucleic acid) synthesis (S), Gap 2(G2) and mitosis (M). In response to DNA damage, telomere‐shortening proliferating cells enter the quiescence phase (G0) in which DNA is repaired. If DNA is repaired, the cell can reenter the cell cycle. However, if DNA has double‐strand DNA damage, cellular senescence appears. Thus, cellular senescence is a cell cycle process in which abnormal, DNA‐damaged or ageing cells are gripped irreversibly and permanently during cell cycle as a common stress reaction. Cellular senescence is of five groups according to initiating factor of senescence: replicative senescence, metabolic stress‐induced senescence, DNA damage‐induced senescence, Fas ligand‐induced senescence and oncogene‐induced senescence. Moreover, there are some biomarkers such as p53, p21, mTOR (mechanistic target of rapamycin), ATM/ATR and pRB for senescence. However, the molecular mechanism underlying senescence has been revealed; however, answers have not arisen regarding the precise nature and physiological significance of the senescence for years. Thus, these processes are highlighted in which recent studies of cell cycle events might need to be reviewed with recent molecular studies of senescence by emphasising the key molecular players, p53 and p53‐dependent players.

Key Concepts

  • What is cell cycle and life?
  • Why do cells choose senescence or quiescence or apoptosis?
  • How do cells choose senescence?
  • When do cells choose senescence?
  • Which cells choose senescence?
  • Which important hallmarks do change during cellular apoptosis?
  • Which physiological things do occur during cellular apoptosis?
  • Does the alteration of senescence cause pathological situations?

Keywords: senescence; cell cycle arrest; cell cycle; quiescence; autophagy; apoptosis; p53

Figure 1. Cellular senescence happens in two phases, mortality stages 1 (M1) and mortality stages 2 (M2), in human fibroblasts.
Figure 2. Launchers for senescence and the changes of senescent cells.
Figure 3. mTOR and p53.
Figure 4. The relation of p53, pRB.
Figure 5. Senescence in cell life.
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Further Reading

Dimri M and Dimri GP (2014) Cancer and the ageing process. In: eLS. John Wiley & Sons, Ltd: Chichester. DOI: 10.1002/9780470015902.a0025372.

Grignolio A and Franceschi C (2012) History of research into ageing/senescence. In: eLS. John Wiley & Sons, Ltd: Chichester. DOI: 10.1002/9780470015902.a0023955.

Rattan IS (2012) Cell senescence in vitro. In: eLS. John Wiley & Sons, Ltd: Chichester. DOI: 10.1002/9780470015902.a0002567.pub3.

Toussaint O, Salmon M, Pascal T, Magalhaes JP and Chainiaux F (2005) Stress induced premature senescence (SIPS). In: eLS. Chichester: John Wiley & Sons, Ltd. DOI: 10.1038/npg.els.0003865.

Terzi MY, Izmirli M and Gogebakan B (2016) The cell fate: senescence or quiescence. Molecular Biology Reports 43 (11): 1213–1220.

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Izmirli, Muzeyyen(Oct 2017) In Cellular Senescence, the Third Circle of the Cell Life's Network, p53 Acts Vital Role. In: eLS. John Wiley & Sons Ltd, Chichester. http://www.els.net [doi: 10.1002/9780470015902.a0027360]