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?