The tumor suppressor p53 is regarded as the guardian of the genome. p53 is activated by various stress signals, such as ribosomal stress, DNA damage, hypoxia, and nutrient depletion. p53 can prevent tumorigenesis by inducing cellular senescence, regulating metabolism, migration and epithelial-mesenchymal transition, blocking metastasis, stopping cell proliferation, ferroptosis and inducing apoptosis, mainly via its transcriptional activity. The E3 ubiquitin ligase MDM2, encoded by a transcriptional target gene of p53 that is often amplified in cancer, is the master negative regulator of p53.

In more than 50% of human cancers the p53 is mutated or deleted, which not only abrogates the tumor suppressive function of wild-type p53, but also mutant proteins with dominant-negative activity. In particular, several hotspot mutants are able to promote cancer progression and resistance to anti-cancer therapies.

We invite all scientists working on p53 to participate in this Special Issue. Original research articles or reviews on all aspects of the molecular and cellular mechanisms modulated by p53 are welcome.

Potential topics include but are not limited to the following:

• Cancers, inflammatory processes, and new biomarkers
• Regulation of immunological research in cancer by p53 activation
• Regulation of immune system and colon diseases by p53 activation
• Regulation of p53 by novel genes
• Regulation of p53 by ribosomal proteins
• Regulation of epithelial-mesenchymal-transition
• Regulation of cell migration and stem cell division