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J. Biol. Chem., Vol. 277, Issue 21, 18528-18534, May 24, 2002
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From the Kv1.3 channels regulate proliferation of normal
lymphocytes, but the role of voltage-gated potassium channels in
transformed hematopoietic cells is not known. We examined transcripts
for Kv1.3, h-erg, h-eag, and
BEC1 genes in primary lymphocytes and leukemias and in
several hematopoietic cell lines. Surprisingly, BEC1,
formerly thought to be brain-specific, was present in all the primary
leukemias examined, in resting peripheral blood lymphocytes, and in
proliferating activated tonsillar cells, lymphocytes from Sjögren's patients, and Epstein-Barr virus-transformed B-cells. Only h-erg mRNA was up-regulated in the cancer cells,
but this was not due to proliferation per se, because it
was not elevated in any of the proliferating noncancerous lymphocyte
types examined. Nor did h-erg transcript levels correlate
with the B-cell subset, because it was elevated in immature neoplastic
B-CLL cells (CD5+) and in a CD5
Functional Up-regulation of HERG K+ Channels in
Neoplastic Hematopoietic Cells*
,,§¶,,,
**, and§**
Division of Cellular and Molecular Biology,
Toronto Western Research Institute, Toronto, Ontario M5T 2S8, Canada
and the Departments of § Physiology and Immunology,
University of Toronto, Ontario M5S 1A8, Canada
Burkitt's
lymphoma cell line (Raji) but not in Sjögren's syndrome cells
(enriched in CD5+ B-cells) or Epstein-Barr
virus-transformed B-cells, which are mature CD5 B-cells.
The protein and whole cell current levels roughly corresponded with the
amount of mRNA expressed in three hematopoietic cell lines: CEM (an
acute lymphoblastic leukemic line), K562 (a chronic myelogenous
leukemic line), and U937 (an acute promyelocytic leukemic line). The
selective HERG channel blocker, E-4031, reduced proliferation of CEM,
U937, and K562 cells, and this appears to be the first direct evidence
of a functional role for the HERG current in cancer cells. Selective
up-regulation of h-erg appears to occur in neoplastic hematopoietic cells, thus providing a marker and potential therapeutic target.
*
This work was funded by Grant MT-13657 from the Canadian
Institutes for Health Research (formerly the Medical Research Council) (to L. C. S.), by a grant from the Natural Sciences and
Engineering Research Council of Canada, and by Grant 11044 from the
National Cancer Institute of Canada (to F. W. L. T).The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.
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