Mutant p53 hinges between epithelial-mesenchymal transition and cancer stem cells

Received: June 03, 2018; Accepted: June 20, 2018; Published: June 23, 2018 Increasing body of evidence ascribes tumorigenesis to the emergence of cancer stem cells (CSCs). The two main theories predicting the origin of CSCs are either transformation of adult stem cells, or dedifferentiation of mature cells that is accompanied by the induction of the epithelial to mesenchymal transition (EMT) program [1]. Yet, both are associated with the accumulation of genetic and epigenetic aberrations that underlies cell plasticity [2]. Since accumulating data link mutations in the tumor-suppressor p53 with both CSCs formation and cancer-associated EMT, it is tempting to hypothesize that mutant p53 might facilitate CSCs formation by inducing EMT and cell plasticity. Here, we will evaluate the latter hypothesis by analyzing recent publications, and supporting it by our new data pertaining prostate cancer.