p21Cip1 Confers resistance to imatinib in human chronic myeloid leukemia cells

被引：17

作者：

Ferrandiz, Nuria ^{[1
]}

Caraballo, Juan M. ^{[1
]}

Albajar, Marta ^{[1
,2
]}

Teresa Gomez-Casares, M. ^{[3
]}

Lopez-Jorge, Carmen E. ^{[3
]}

Blanco, Rosa ^{[1
]}

Dolores Delgado, M. ^{[1
]}

Leon, Javier ^{[1
]}

机构：

[1] Univ Cantabria, Dept Biol Mol, Inst Biomed & Biotecnol Cantabria IBBTEC, CSIC IDICAN, Santander 39011, Spain

[2] Hosp Univ Marques Valdecilla IFIMAV, Serv Hematol, Santander, Spain

[3] Hosp Dr Negrin, Hematol Serv, Unidad Biol Mol, Las Palmas Gran Canaria, Spain

来源：

CANCER LETTERS | 2010年 / 292卷 / 01期

关键词：

p21; Imatinib; Chronic myeloid leukemia; Apoptosis; CHRONIC MYELOGENOUS LEUKEMIA; PHILADELPHIA-CHROMOSOME; TUMOR SUPPRESSION; INHIBITOR P21; P21(WAF1/CIP1); EXPRESSION; APOPTOSIS; MICE; LINE; ACTIVATION;

D O I：

10.1016/j.canlet.2009.11.017

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

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. (C) 2009 Elsevier Ireland Ltd. All rights reserved.

引用

页码：133 / 139

页数：7

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