View the Current Issue

Article

  • The EMBO Journal (1999) 18, 5540 - 5547
  • doi:10.1093/emboj/18.20.5540

Oncogenic potential of EAG K+ channels

Luis A. Pardo1, Donato del Camino2, Araceli Sánchez1, Frauke Alves3, Andrea Brüggemann4, Synnöve Beckh1 and Walter Stühmer1

  1. Max-Planck-Institut für experimentelle Medizin, Hermann-Rein-Strasse 3, D-37075 Göttingen, Germany
  2. Present address: Neurobiology Department, Harvard Medical School, Boston, MA 02115, USA
  3. Abteilung Hämatologie und Onkologie, Universitätsklinikum Göttingen, Göttingen, Germany
  4. Present address: Hoechst-Marion-Roussel, DG Cardiovascular, H821, D-65926 Frankfurt, Germany

Correspondence to:

Luis A. Pardo, E-mail: pardo@mail.mpiem.gwdg.de

Received 31 May 1999; Accepted 24 August 1999; Revised 10 August 1999

We have investigated the possible implication of the cell cycle-regulated K+ channel ether à go-go (EAG) in cell proliferation and transformation. We show that transfection of EAG into mammalian cells confers a transformed phenotype. In addition, human EAG mRNA is detected in several somatic cancer cell lines, despite being preferentially expressed in brain among normal tissues. Inhibition of EAG expression in several of these cancer cell lines causes a significant reduction of cell proliferation. Moreover, the expression of EAG favours tumour progression when transfected cells are injected into immune-depressed mice. These data provide evidence for the oncogenic potential of EAG.

  • Keywords:

    • ether à go-go,
    • K+ channels,
    • proliferation,
    • transformation