Abstract
Mutant p53 is frequently detected in cancers in which p53 has lost its ability in tumor suppression and gained function in promoting tumor progression. Restoration of p53 functions by replacement of wild-type p53 and inhibition of its degradation or increment of its transcriptional activity has been applied to the prevention and treatment of cancers. Recent evidence indicates that disrupting ceramide glycosylation can resuscitate wild-type p53 expression and p53-dependent apoptosis in mutant p53 tumors. A posttranscriptional process that can turn on wild-type p53 expression and abrogate mutant p53 may provide a new strategy to eradicate mutant p53 cancers.