p53 is among the most critical tumor suppressor genes and is the most extensively studied gene in tumor biology in the past 40 years. Due to its multiple functions in tumor formation, p53 has been recognized as quite a promising target to treat cancer. In order to leverage the crucial roles of p53 in tumor therapy, we need to figure out the exact mechanism for p53 function and how is p53 regulated. Conventional activities of p53 such as cell cycle arrest, senescence, and apoptosis are well accepted as the major checkpoints in stress responses. However, accumulating evidence implicates the importance of other tumor suppression mechanisms, including regulating cancer cell metabolism, ferroptosis, and stemness. Besides its crucial role in tumor biology, p53 is also demonstrated to function in various physiological and pathological processes, such as obesity, aging, and immune response.
By launching this research topic, we wish to collect manuscripts about the emerging roles of p53 in mediating cell metabolism, ferroptosis, and stemness, which link p53 with diverse diseases, particularly tumors. Elucidating the mechanism of p53 in regulating these cellular activities will not only benefit the basic research of p53 and tumor biology but also open promising doors for developing therapeutics targeting p53 and related pathways for the treatment of cancer and other diseases.
Submissions including Original Research Articles, Reviews, and Mini-Reviews are welcome to this Research Topic. Papers are expected to cover but are not limited to the following topics:
(1) How p53 regulates cell metabolism, ferroptosis, and stemness in diverse physiological and pathological settings.
(2) Genetic and epigenetic alterations in the p53 gene and its consequence in diseases. Research about mutant p53 are particularly welcome.
(3) Targeting p53 and associated factors/pathways for disease treatment.
(4) All the above topics apply to papers related to p53 family members p63 and p73.
Please note that the findings based on bioinformatic data mining should be biologically validated by in vitro and/or in vivo experiments.
p53 is among the most critical tumor suppressor genes and is the most extensively studied gene in tumor biology in the past 40 years. Due to its multiple functions in tumor formation, p53 has been recognized as quite a promising target to treat cancer. In order to leverage the crucial roles of p53 in tumor therapy, we need to figure out the exact mechanism for p53 function and how is p53 regulated. Conventional activities of p53 such as cell cycle arrest, senescence, and apoptosis are well accepted as the major checkpoints in stress responses. However, accumulating evidence implicates the importance of other tumor suppression mechanisms, including regulating cancer cell metabolism, ferroptosis, and stemness. Besides its crucial role in tumor biology, p53 is also demonstrated to function in various physiological and pathological processes, such as obesity, aging, and immune response.
By launching this research topic, we wish to collect manuscripts about the emerging roles of p53 in mediating cell metabolism, ferroptosis, and stemness, which link p53 with diverse diseases, particularly tumors. Elucidating the mechanism of p53 in regulating these cellular activities will not only benefit the basic research of p53 and tumor biology but also open promising doors for developing therapeutics targeting p53 and related pathways for the treatment of cancer and other diseases.
Submissions including Original Research Articles, Reviews, and Mini-Reviews are welcome to this Research Topic. Papers are expected to cover but are not limited to the following topics:
(1) How p53 regulates cell metabolism, ferroptosis, and stemness in diverse physiological and pathological settings.
(2) Genetic and epigenetic alterations in the p53 gene and its consequence in diseases. Research about mutant p53 are particularly welcome.
(3) Targeting p53 and associated factors/pathways for disease treatment.
(4) All the above topics apply to papers related to p53 family members p63 and p73.
Please note that the findings based on bioinformatic data mining should be biologically validated by in vitro and/or in vivo experiments.
