The phosphoinositide 3-kinase/Akt pathway is essential for the retinoic acid-induced differentiation of F9 cells.

Date publication

mars 2006

Auteurs

Membres identifiés du Cancéropôle Est :
Dr ROCHETTE-EGLY Cécile

Tous les auteurs :
Bastien J, Plassat JL, Payrastre B, Rochette-Egly C

Lien Pubmed

https://www.ncbi.nlm.nih.gov/pubmed/16288212

Résumé

Retinoic acid (RA) induces cell growth arrest and differentiation through two families of nuclear receptors, the RARs and the RXRs. The phosphoinositide 3-kinase (PI3K)/Akt pathway also plays key roles in these processes, that is, cell cycle progression, cell differentiation and cell survival. We report that, in mouse embryocarcinoma cells (F9 cells), RA induces an early activation of PI3K and Akt via an increase in the expression of the p85alpha regulatory subunit. This effect is followed by an inhibition of Akt. Both effects require the integrity of the RA pathway as they are not observed in RA-resistant RARgamma null cells. We propose a model through which RA induces a biphasic regulation of Akt with an activation participating to the differentiation process, followed by an inhibition, which has been correlated to the RA-induced growth arrest.

Référence

Oncogene. 2006 Mar 30;25(14):2040-7.