Targeting MDM4 Splicing in Cancers
AbstractMDM4, 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. View Full-Text
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Bardot, B.; Toledo, F. Targeting MDM4 Splicing in Cancers. Genes 2017, 8, 82.
Bardot B, Toledo F. Targeting MDM4 Splicing in Cancers. Genes. 2017; 8(2):82.Chicago/Turabian Style
Bardot, Boris; Toledo, Franck. 2017. "Targeting MDM4 Splicing in Cancers." Genes 8, no. 2: 82.
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