Opposing Roles of Wild-type and Mutant p53 in the Process of Epithelial to Mesenchymal Transition

The central role of an aberrantly activated EMT program in defining the critical features of aggressive carcinomas is well documented and includes cell plasticity, metastatic dissemination, drug resistance, and cancer stem cell-like phenotypes. The p53 tumor suppressor is critical for leashing off all the features mentioned above. On the molecular level, the suppression of these effects is exerted by p53 via regulation of its target genes, whose products are involved in cell cycle, apoptosis, autophagy, DNA repair, and interactions with immune cells. Importantly, a set of specific mutations in the TP53 gene (named Gain-of-Function mutations) converts this tumor suppressor into an oncogene. In this review, we attempted to contrast different regulatory roles of wild-type and mutant p53 in the multi-faceted process of EMT.

Automated summary

The aberrantly activated EMT program plays a central role in defining the critical features of aggressive carcinomas, and the p53 gene is critical for suppressing these features. Specific mutations in the p53 gene can convert it into an oncogene. This review contrasts the different regulatory roles of wild-type and mutant p53 in the process of EMT.