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Article Dans Une Revue Cell Cycle Année : 2010

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

Résumé

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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Dates et versions

inserm-00512728 , version 1 (31-08-2010)

Identifiants

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

Citer

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