Abstract
TP53 is one of the most frequently-mutated and deleted tumor suppressors in cancer, with a dramatic correlation with dismal prognoses. In addition to genetic inactivation, the p53 protein can be functionally inactivated in cancer, through post-transductional modifications, changes in cellular compartmentalization, and interactions with other proteins. Here, we review the mechanisms of p53 functional inactivation, with a particular emphasis on the interaction between p53 and IκB-α, the NFKBIA gene product.
Highlights
TP53 is the most renowned tumor suppressor among clinicians and researchers, and is one of the most extensively studied [1,2,3,4]
The role of p53 in cancer should include the following, novel, non-canonical functions: (i) various TP53 mutations behave as gain of functions [1,17,18,19,20]; (ii) the p53 protein is no longer just a transcriptional factor [21,22,23,24], but acts in different cellular compartments outside the nucleus, where it mediates several processes through a complex network of partners [25,26,27,28]; (iii) wild-type p53 should result in being functionally inactive through changes in compartmentalization or protein modifications [29,30,31]; and (iv) non-cell-autonomous tumor suppression properties of p53 have been discovered [32]
P53 inactivation allows for the design of novel therapies that are able to promote its re-activation, with for the design of novel therapies that are able to promote its re-activation, with the important induction of cancer selective apoptosis
Summary
TP53 is the most renowned tumor suppressor among clinicians and researchers, and is one of the most extensively studied [1,2,3,4]. Mechanisms of p53 Functional De-Regulation: Role of the IκB-α/p53 Complex We review the mechanisms of p53 functional inactivation, with a particular emphasis on the interaction between p53 and IκB-α, the NFKBIA gene product.
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