ICBP90 mediates the ERK1/2 signaling to regulate the proliferation of Jurkat T cells.
Fiche publication
Date publication
janvier 2009
Auteurs
Membres identifiés du Cancéropôle Est :
Dr BRONNER Christian
Tous les auteurs :
Fang Z, Xing F, Bronner C, Teng Z, Guo Z
Lien Pubmed
Résumé
ERK1/2 activation leads to the release of E2F that could bind to the E2F binding sites in the inverted CCAAT box binding protein (ICBP90) gene promoter. Therefore, in the present study the relationship between ERK1/2 signaling and ICBP90 in the regulation of Jurkat T cell proliferation was explored. Jurkat T cells were treated with different concentrations of various signal pathway inhibitors. The cell viability and cell cycle were determined. Furthermore, the expression of non-phosphorylated and phosphorylated ERK1/2, and ICBP90 was measured by Western blot analysis. All the inhibitors, including PD98059, LY294002, AG490, genistein and GF109203X, suppressed the cell colony formation and proliferation to different extent in a dose-dependent manner. PD98059 could suppress the cell proliferation remarkably, arrested the cell cycle at G1/G0 stage and blocked its entrance from S phase to G2/M phase. Three or 24h after exposure to the inhibitors, all the inhibitors downregulated the level of the phosphorylated ERK1/2, of which the inhibitory roles of PD98059, LY294002 and AG490 were more significant. All the inhibitors had no effect on the expression of ICBP90 after 3h treatment, but downregulated markedly its expression after 24h treatment, especially PD98059, LY294002 and AG490. The expression of ICBP90 was directly proportioned to the level of ERK1/2 phosphorylation and the cell proliferation. Our results demonstrate that ICBP90 might be a pivotal target for the ERK1/2 signaling pathway to control the proliferation of Jurkat T cells.
Référence
Cell Immunol. 2009;257(1-2):80-7