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Blood, Vol. 94 No. 1 (July 1), 1999:
pp. 139-145
A Requirement for K+-Channel Activity in Growth
Factor-Mediated Extracellular Signal-Regulated Kinase Activation in
Human Myeloblastic Leukemia ML-1 Cells
Dazhong Xu,
Ling Wang,
Wei Dai, and
Luo Lu
From the Department of Physiology and Biophysics, School of Medicine,
Wright State University, Dayton; and the Division of Hematology,
Department of Medicine, University of Cincinnati College of Medicine,
Cincinnati, OH.
Voltage-gated K+ channels have been shown to be
required for proliferation of various types of cells. Much evidence
indicates that K+-channel activity is required for
G1 progression of the cell cycle in different cell
backgrounds, suggesting that K+-channel activity is
required for early-stage cell proliferation in these cells. However,
little is known about the molecular mechanisms that underlie this
phenomenon. We have shown in human myeloblastic leukemia ML-1 cells
that K+ channels are activated by epidermal growth factor
(EGF), whereas serum starvation deprivation suppressed their activity.
In addition, voltage-gated K+ channels are required for
G1/S-phase transition of the cell cycle. We report here
that suppression of K+ channels prevented the activation
of extracellular signal-regulated protein kinase 2 (ERK-2) in response
to EGF and serum. However, blockade of K+ channels did
not prevent ERK-2 activation induced by 12-O-tetradecanoyl-phorbol 13-acetate (TPA). Elimination of extracellular Ca2+ did
not alter either ERK-2 activation or the effect of
K+-channel blockade on ERK-2 activation. Our data
demonstrate that the K+ channel is a part of the
EGF-mediated mitogenic signal-transduction process and is required for
initiation of the EGF-mediated mitogen-activated protein kinase (MAPK)
pathways. Our findings may thus explain why an increase in
K+-channel activity is associated with cell proliferation
in many types of cells, including ML-1 cells.
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