Resumen
This article describes an emerging area of significant interest in cancer and cell death and the relationships shared by these through the p53 and cathepsin proteins. While it has been demonstrated that the p53 protein can directly induce the leakage of cathepsin proteases from the lysosome, directly triggering cell death, little is known about what factors set the threshold at which the lysosome can become permeabilized. It appears that the expression levels of cathepsin proteases may be central to this process, with some of them being transcriptionally regulated by p53. The consequences of such a mechanism have serious implications for lysosomal-mediated apoptosis and have significant input into the design of therapeutics and their strategic use. In this review, we highlight the importance of extending such findings to other cathepsin family members and the need to assess the roles of p53 isoforms and mutants in furthering this mechanism.