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p53 is a signaling molecule that orchestrates smart responses to diverse stimuli and employs temporal dynamics for the selective activation of downstream target genes and ultimately for cell fate decisions. Emerging evidences support that the tumor suppressor p53 is the most frequently mutated protein in human cancers. However, it remains elusive how to regulate cell fate decisions and control the direction of cell fates. In this paper, we aim to study the effects of drug dose, the drug frequency, and the drug time on the cell fate decisions of the system. We find that a certain dose of the drug can indeed change the fate of the p53 system, initiate DNA repair procedures, and ultimately allow the cells to survive. Compared with the single dose, the multiple use of the drug not only greatly reduces the dose, but also can more quickly initiate the repair mechanism of the p53 system. We also find that taking medicine at the trough of p53 concentration requires more medication so that the number of pulses is below the threshold. However, the dose is greatly reduced if we take medicine at the peak. All of these results are very meaningful in the treatment of cancer.

Chronotherapy for the p53 system under DNA damage response