Author/Authors :
Ferrandiz، نويسنده , , Nuria and Caraballo، نويسنده , , Juan M. and Albajar، نويسنده , , Marta and Teresa Gomez-Casares، نويسنده , , M. and Lopez-Jorge، نويسنده , , Carmen E. and Blanco، نويسنده , , Rosa and Dolores Delgado، نويسنده , , M. and Leon، نويسنده , , Javier، نويسنده ,
Abstract :
Imatinib is a Bcr-Abl inhibitor used as first-line therapy of chronic myeloid leukemia (CML). p21Cip1, initially described as a cell cycle inhibitor, also protects from apoptosis in some models. We describe that imatinib down-regulates p21Cip1 expression in CML cells. Using K562 cells with inducible p21 expression and transient transfections we found that p21 confers partial resistance to imatinib-induced apoptosis. This protection is not related to the G2-arrest provoked by p21, a decrease in the imatinib activity against Bcr-Abl or a cytoplasmic localization of p21. The results suggest an involvement of p21Cip1 in the response to imatinib in CML.
Keywords :
p21 , Imatinib , apoptosis , Chronic myeloid leukemia
