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J Biol Chem, Vol. 275, Issue 10, 7189-7197, March 10, 2000
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From the The mitogen-activated protein kinase ERK1/2
pathway is essential in the control of cell proliferation and
differentiation in most cellular systems. As such, it has been
considered a potential target for antineoplastic therapy. For this
purpose, we have examined the role of ERK activation in myeloid
leukemia cell growth and differentiation. Using a representative set of
myeloid leukemia cell lines, we show that cell proliferation was not
accompanied by increases on ERK1/2 activation, and mitogenic
stimulation did not enhance ERK activity. Moreover, abolition of ERK
function by the inhibitor PD98059 or by a dominant inhibitory mutant
ERK2 had no significant effects on proliferation. With the aid of
various differentiation inducers, we found that within the same cell
line, differentiation to a given lineage could occur with and without ERK1/2 activation, depending on the stimulus. Also, a differentiator could have the same effect in the presence or absence of ERK
stimulation, depending on the cell line. ERK inhibition did not affect
the differentiation elicited by stimuli whose effects were accompanied by ERK activation. Finally, constitutive ERK activity was also ineffective on proliferation and differentiation. Thus, our results indicate that ERK1/2 activation is not an essential requirement for
leukemic cell growth and differentiation.
Unidad de Biología Molecular del
Cáncer, Departamento de Biología Molecular, Universidad
de Cantabria, Santander 39011, the ¶ Instituto de Investigaciones
Biomédicas, Consejo Superior de Investigaciones
Centíficas, Madrid 28029, and § Servicio de
Hematología, Hospital Universitario Marqués de Valdecilla
Santander 39010, Spain
To whom correspondence should be addressed: Instituto de
Investigaciones Biomédicas, Consejo Superior de Investigaciones Centíficas, Arturo Duperier 4, Madrid 28029, Spain. Tel.:
34-91-5854886; Fax: 34-91-5854587; E-mail: pcrespo@iib.uam.es.
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