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Published online before print August 29, 2006

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(Journal of Leukocyte Biology. 2006;80:1473-1479.)
© 2006 by Society for Leukocyte Biology

Regulation of Akt/PKB by phosphatidylinositol 3-kinase-dependent and -independent pathways in B-cell chronic lymphocytic leukemia cells: role of protein kinase Cβ

Montserrat Barragán^*,1, Mercè de Frias^*,1, Daniel Iglesias-Serret^*, Clara Campàs^*, Esther Castaño^*, Antonio F. Santidrián^*, Llorenç Coll-Mulet^*, Ana M. Cosialls^*, Alicia Domingo, Gabriel Pons^* and Joan Gil^*,2

^* Unitat de Bioquímica, Departament de Ciències Fisiològiques II, IDIBELL-Universitat de Barcelona, Campus de Bellvitge, L’Hospitalet de Llobregat, Barcelona, Spain; and
Servei d’Hematologia, IDIBELL-Hospital Universitari de Bellvitge, Campus de Bellvitge, L’Hospitalet de Llobregat, Barcelona, Spain

² Correspondence: Departament de Ciències Fisiològiques II, IDIBELL-Universitat de Barcelona, Campus de Bellvitge, Pavelló de Govern, 4ª planta, L’Hospitalet de Llobregat, Barcelona E-08907, Spain. E-mail: jgil{at}ub.edu

Apoptosis of B cell chronic lymphocytic leukemia (B-CLL) cells is regulated by the PI-3K-Akt pathway. In the present work, we have analyzed the mechanisms of Akt phosphorylation in B-CLL cells. Freshly isolated cells present basal Akt phosphorylation, which is PI-3K-dependent, as incubation with the PI-3K inhibitor LY294002 decreased Ser-473 and Thr-308 phosphorylation in most samples analyzed (seven out of 10). In three out of 10 cases, inhibition of protein kinase C (PKC) inhibited basal Akt phosphorylation. Stromal cell-derived factor-1, IL-4, and B cell receptor activation induced PI-3K-dependent Akt phosphorylation. PMA induced the phosphorylation of Akt at Ser-473 and Thr-308 and the phosphorylation of Akt substrates, independently of PI-3K in B-CLL cells. In contrast, PKC-mediated phosphorylation of Akt was PI-3K-dependent in normal B cells. Finally, a specific inhibitor of PKCβ blocked the phosphorylation and activation of Akt by PMA in B-CLL cells. Taken together, these results suggest a model in which Akt could be activated by two different pathways (PI-3K and PKCβ) in B-CLL cells.

Key Words: apoptosis • signal transduction

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