1.
J Renin Angiotensin Aldosterone Syst
; 14(1): 91-2, 2013 Mar.
Artigo
em Inglês
| MEDLINE
| ID: mdl-23418283
2.
Cancer Lett
; 292(1): 133-9, 2010 Jun 01.
Artigo
em Inglês
| MEDLINE
| ID: mdl-20042273
RESUMO
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.