Control of contact-inhibition by 4E-BP1 upregulation.

Abstract : Although contact inhibition is a fundamental process for multicellular organisms, how proliferation is inhibited at high cellular densities remains poorly characterized. Here we show that 4E-BP1, one major repressor of cap-dependent translation, plays a critical role in density-mediated cell cycle arrest. 4E-BP1 promoter is activated and 4E-BP1 protein amount increases as cells reach confluence. Conversely, a much less marked density-dependent inhibition of cell proliferation is observed upon 4E-BP1 silencing. We further show that at high density, progression through the G(1) phase of the cell cycle is faster and Cyclin D1 protein is induced in different cell types where 4E-BP1 has been either downregulated (stable shRNA expression or transient siRNA transfection) or removed (knockout). Thus 4E-BP1 appears as an important mediator of contact inhibition.
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Article dans une revue
Cell Cycle, Taylor & Francis, 2010, 9 (7), epub ahead of print
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http://www.hal.inserm.fr/inserm-00512728
Contributeur : Marie Francoise Simon <>
Soumis le : mardi 31 août 2010 - 14:21:16
Dernière modification le : mercredi 1 septembre 2010 - 10:21:24

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  • HAL Id : inserm-00512728, version 1
  • PUBMED : 20372058

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Rania Azar, Christiane Susini, Corinne Bousquet, Stéphane Pyronnet. Control of contact-inhibition by 4E-BP1 upregulation.. Cell Cycle, Taylor & Francis, 2010, 9 (7), epub ahead of print. 〈inserm-00512728〉

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