1.Apoptosis is a complex program that often depends on mitochondria and is irreversible.

2.“cell cycle arrest,” often called “growth arrest”) can be either irreversible (“senescence”) or reversible (“return to proliferation”).

3.They all can be regulated by p53.

4.In my opinion, the two concepts are like :"my company is bankrupt" and "the income of my company is zero".

5.The attachment is a paper to describe the details (molecular regulation) of the two concepts, please see more information in that article.

1.Apoptosis is a complex program that often depends on mitochondria and is irreversible.

2.“cell cycle arrest,” often called “growth arrest”) can be either irreversible (“senescence”) or reversible (“return to proliferation”).

3.They all can be regulated by p53.

4.In my opinion, the two concepts are like :"my company is bankrupt" and "the income of my company is zero".

5.The attachment is a paper to describe the details (molecular regulation) of the two concepts, please see more information in that article.

Rama,

Cell cycle denotes the organization and sequence of steps in the cell through which a cell’s chromosomes undergo duplication and division into two. Cell cycles in a majority of eukaryotes can be divided into four phases, G1 (prior to DNA replication), S (DNA replication), G2 (post-DNA synthesis) and M (phase during which cell division occurs, producing two daughter cells). The daughter cells, now in the G1 phase, will then pass through another cycle depending on external conditions. When they remain in G1 phase for prolonged periods of time they arrest as quiescent, non-dividing cells in a G0 phase before recommencing DNA synthesis.  Even though they are metabolically active they do not actively proliferate. Proper stimulation of these cells induces them to revert to the G1 phase and resume growth and division.

One of the principal checkpoints that regulates the transition from G0/G1 to S phase is termed the restriction point (R). Induction of apoptosis is a critical response to nuclear DNA damage.  Upon sensing impending DNA damage, normal cells in G1 phase prior to the R point would arrest in G1 phase. If cells in G2 phase sense DNA damage a G2 cell-cycle arrest would then ensue.  

Apoptosis, which has also been sometimes termed as programmed cell death, is a process to accomplish cell suicide, which endows multicellular organisms with the ability to regulate cell number in tissues and to eliminate unwanted or aging cells during the course of development of an organism. The apoptosis pathway comprises an array of positive and negative regulators of proteases called caspases, which cleave several substrates. Furthermore, apoptosis is characterized by the intranucleosomal degradation of chromosomal DNA, producing the characteristic DNA ladder observed for chromatin isolated from cells undergoing apoptosis. During the early stages of apoptosis, dense chromosome condensation occurs along the nuclear periphery. While most organelles remain intact the cell body shrinks. Subsequently, both the nucleus and cytoplasm fragment and form apoptotic bodies, which are phagocytosed by surrounding cells.

Best regards...  

As Bingxian has indicated, p53 is involved in both cell cycle arrest and apoptosis. The p53 gene product is a crucial cell-cycle checkpoint regulator at both the G1/S and G2/M. The p53 tumor-suppressor gene is the most frequently mutated gene in human cancer, highlighting its potentially important role in conserving normal cell-cycle progression. One of the essential functions of p53 is to arrest cells in the G1 phase upon sensing DNA damage, and to allow for DNA repair prior to DNA replication and cell division. In response to excessive and massive DNA damage, p53 triggers the apoptotic cell death pathway.

The available research evidence says that manipulation of the cell cycle may either prevent or induce an apoptotic response.

Ref Link: Pucci, B., Kasten, M., & Giordano, A. (2000). Cell Cycle and Apoptosis. Neoplasia (New York, N.Y.), 2(4), 291–299.

Regards

Dr. Kamath Madhusudhana