targeting mdm4 splicing in cancers

Clicks: 252
ID: 182998
2017
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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.
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bardot2017genestargeting mdm4 splicing in cancers Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors ;Boris Bardot;Franck Toledo
Journal thermal science and engineering progress
Year 2017
DOI
10.3390/genes8020082
URL
http://www.mdpi.com/2073-4425/8/2/82
Keywords
alternative splicing p53

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