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Genes 2017, 8(2), 82;

Targeting MDM4 Splicing in Cancers

Génétique de la Suppression Tumorale, Equipe Labellisée Ligue, Institut Curie, Centre de Recherche,  Sorbonne Universités, UPMC Univ Paris 06, CNRS UMR 3244, PSL Research University, 26 rue d’Ulm,   75248 Paris CEDEX 05, France 
Authors to whom correspondence should be addressed.
Received: 8 November 2016 / Accepted: 15 February 2017 / Published: 20 February 2017
(This article belongs to the Special Issue Therapeutic Alternative Splicing: Mechanisms and Applications)
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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. View Full-Text
Keywords: MDM4; MDM2; p53; alternative splicing; isoform MDM4; MDM2; p53; alternative splicing; isoform
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

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Bardot, B.; Toledo, F. Targeting MDM4 Splicing in Cancers. Genes 2017, 8, 82.

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