Antiopoptotic proteins Bc12 and Bc1X do not protect chronic myeloid leukemia cells from imatinib-mediated growth arrest

• Autores: María Teresa Gómez Casares, José Pedro Vaqué Díez, Angelina Lemes, Teresa Molero, Nuria Ferrándiz, Javier León
• Localización: Anales de la Real Academia Nacional de Farmacia, ISSN-e 1697-4298, ISSN 0034-0618, Nº. 4 1, 2006, págs. 27-36
• Idioma: español
• Títulos paralelos:
  • Antiapoptotic proteins Bcl2 and BclX do not protect chronic myeloid leukemia cells from imatinib-mediated growth arrest
• Texto completo no disponible (Saber más ...)
• Resumen

  • 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 BclXcell 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.