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Originally published In Press as doi:10.1074/jbc.M210789200 on November 12, 2002

J. Biol. Chem., Vol. 278, Issue 5, 2947-2955, January 31, 2003
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Cell Cycle-dependent Expression of HERG1 and HERG1B Isoforms in Tumor Cells*

Olivia CrocianiDagger , Leonardo GuastiDagger , Manuela Balzi§, Andrea Becchetti, Enzo Wanke, Massimo OlivottoDagger , Randy S. Wymore||, and Annarosa ArcangeliDagger **

From the Dagger  Department of Experimental Pathology and Oncology, University of Firenze, Viale G. B. Morgagni 50, 50134 Firenze, Italy, the || Department of Biological Science, University of Tulsa, Tulsa, Oklahoma 74104-3189, the § Department of Clinical Physiopathology, University of Firenze, Viale Pieraccini 6, 50134 Firenze, and the  Department of Biotechnology and Biosciences, University of Milano Bicocca, Piazza della Scienza 2, 20126 Milano, Italy

The role of K+ channel activity during cell cycle progression has become a research topic of considerable interest. Blocking of K+ channels inhibits the proliferation of many cell types, although the mechanism of this inhibition is unclear. There is speculation that K+ channels differentially regulate the electrical potential of the plasma membrane (Vm) during proliferation. We have demonstrated that in tumor cells the value of Vm is clamped to rather depolarized values by K+ channels belonging to the HERG family. We report here that tumor cell lines preferentially express the herg1 gene and a truncated, N-deleted form that corresponds to herg1b. This alternative transcript is also expressed in human primary acute myeloid leukemias. Both HERG1 and HERG1B proteins are expressed on the plasma membrane of tumor cells and can form heterotetramers. The expression of HERG protein isoforms is strongly cell cycle-dependent, accounting for variations in HERG currents along the mitotic cycle. Moreover, the blocking of HERG channels dramatically impairs cell growth of HERG-bearing tumor cells. These results suggest that modulated expression of different K+ channels is the molecular basis of a novel mechanism regulating neoplastic cell proliferation.

* This work was supported by grants from the Associazione Italiana Contro le Leucemie (Firenze) (to A. A.), Associazione Italiana Contro le Leucemie Comitato 30 ore (to A. A.), from the Ministero dell'Università e Ricerca Scientifica e Tecnologica (MURST, Cofin `99 and Cofin `01) (to A. A.), from the Associazione Italiana per la Ricerca sul Cancro (to M. O.), and from Ente Cassa di Risparmio di Firenze (to M. O.).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.

The nucleotide sequence(s) reported in this paper has been submitted to the GenBankTM/EBI Data Bank with accession number(s) AJ512214.

** To whom correspondence should be addressed: Dept. of Experimental Pathology and Oncology, Viale Morgagni 50, 50134 Firenze, Italy. Tel.: 39-055-4282326; Fax: 39-055-4282333; E-mail: annarosa.arcangeli@unifi.it.

Copyright © 2003 by The American Society for Biochemistry and Molecular Biology, Inc.
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