| Literature DB >> 20042273 |
Nuria Ferrandiz1, Juan M Caraballo, Marta Albajar, M Teresa Gomez-Casares, Carmen E Lopez-Jorge, Rosa Blanco, M Dolores Delgado, Javier Leon.
Abstract
Imatinib is a Bcr-Abl inhibitor used as first-line therapy of chronic myeloid leukemia (CML). p21(Cip1), initially described as a cell cycle inhibitor, also protects from apoptosis in some models. We describe that imatinib down-regulates p21(Cip1) 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 p21(Cip1) in the response to imatinib in CML. Copyright (c) 2009 Elsevier Ireland Ltd. All rights reserved.Entities:
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Year: 2009 PMID： 20042273 DOI： 10.1016/j.canlet.2009.11.017
Source DB: PubMed Journal: Cancer Lett ISSN： 0304-3835 Impact factor: 8.679