Molecular Mechanism of Cross-regulation between DNA Repair and Apoptosis

DNA damage is an inevitable event in cell life activities, and its repair and coping mechanism is the core of maintaining genome stability. When DNA damage occurs, cells activate a complex network of signals that restore genomic integrity through repair mechanisms or initiate programmed apoptosis when the damage is irreversible in order to eliminate potentially harmful cells. The regulation of homeostasis involves several key molecules. As the core molecules regulating these two major processes, tumor suppressor P53 and polyadenosine diphosphoribose polymerase (PARP) play an important role in maintaining genome homeostasis and cell fate determination. In recent years, studies have shown that P53 and PARP form a dynamic balance in DNA damage response through a complex interaction network, and the dysregulation of its regulatory mechanism is closely related to disease progression, especially cancer. This paper aims to systematically elucidate the molecular interaction mechanism between P53 and PARP, explore how they balance cell fate through dynamic synergism or antagonism, and analyze their potential targeting value in tumor therapy. Future studies are needed to further reveal tissue-specific regulatory differences, the effects of epigenetic modifications, and the effects of microenvironmental signals on cross-regulation in order to promote the optimization of individualized treatment programs.