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An. R. Acad. Nac. Farm., 2006, 72: 27-36

Artículo original

Antiapoptotic proteins Bcl2 and BclX do not
protect chronic myeloid leukemia cells from

imatinib-mediated growth arrest

Recibido el 31 de enero de 2006

M. TERESA GÓMEZ-CASARES 1, JOSÉ P. VAQUÉ 2, ANGELINA
LEMES 1, TERESA MOLERO 1, NURIA FERRÁNDIZ 2
Y JAVIER LEÓN 2*

1 Servicio de Hematología, Hospital Dr. Negrín, Las Palmas, Spain
2 Grupo de Biología Molecular del Cáncer, Departamento de Biología

Molecular y Unidad de Biomedicina-CSIC, Universidad de
Cantabria, Santander, Spain

ABSTRACT

Imatinib (Glivec, Gleevec, STI571), a Bcr-Abl kinase inhibitor, is the most used
drug in chronic myeloid leukemia. Imatinib induces apoptosis in a number of
CML-derived cell lines, including K562. However, in order to achieve hematological
remissions it is required chronic treatment with the drug, a fact inconsistent with
a cytotoxic mechanism of imatinib in vivo. In this work we have analysed the
effects of imatinib on the proliferation and apoptosis of K562-derived cell lines
with constitutive expression of the anti-apoptotic genes Bcl2 and BclX. We found
that imatinib-mediated apoptosis was completely abrogated in both Bcl2- and BclX-
cell lines. However, imatinib inhibited proliferation, although growth rate was
higher than in parental K562. We conclude that, besides its apoptotic effect,
imatinib acts through an apoptosis-independent mechanism to arrest cell growth.

Key words: Bcl2.—BclX.—Imatinib.—K562.—CML.

* Corresponding author: Javier León, Departamento de Biología Molecular, Facul-
tad de Medicina, Universidad de Cantabria, 39011 Santander, Spain.

Phone: 34-942-201952; Fax: 34-942-201945; Email: leonj@unican.es
Abbreviations: CML, chronic myeloid leukemia.

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