Exploration of novel regulators of mutant p53 in cancer cells: a role for NDFIP1

Abstract

Mutations in the tumour suppressor gene, TP53 occur in more than 50% of human cancers. Mutant p53 proteins not only lose their tumour suppressive capacities, but also gain oncogenic functions, broadly referred to as gain of function (GOF). Cancer cells frequently accumulate mutant p53 and may become addicted to this protein for their survival. During development, mutant p53, like its wild-type counterpart, is inherently labile, however in cancer cells mutant p53 frequently accumulates. In part, this is due to the interrupted auto-regulatory loop with MDM2. However, MDM2 alone cannot explain the stability of mutant p53 in many cancer contexts. We therefore argued that additional factors are r..