Abstract：
:MDM4, an essential negative regulator of the P53 tumor suppressor, is frequently overexpressed in cancer cells that harbor a wild-type P53. By a mechanism based on alternative splicing, the MDM4 gene generates two mutually exclusive isoforms: MDM4-FL, which encodes the full-length MDM4 protein, and a shorter splice variant called MDM4-S. Previous results suggested that the MDM4-S isoform could be an important driver of tumor development. In this short review, we discuss a recent set of data indicating that MDM4-S is more likely a passenger isoform during tumorigenesis and that targeting MDM4 splicing to prevent MDM4-FL protein expression appears as a promising strategy to reactivate p53 in cancer cells. The benefits and risks associated with this strategy are also discussed.
journal_name
Genes (Basel)journal_title
Genesauthors
Bardot B,Toledo Fdoi
10.3390/genes8020082subject
Has Abstractpub_date
2017-02-20 00:00:00issue
2issn
2073-4425pii
genes8020082journal_volume
8pub_type
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