Research

Overexpression of Eag1 potassium channels in clinical tumours

Bernhard Hemmerlein¹ , Rüdiger M Weseloh² , Fernanda Mello de Queiroz^2,3 , Hendrik Knötgen⁴ , Araceli Sánchez² , María E Rubio² , Sabine Martin^2,5 , Tessa Schliephacke⁴ , Marc Jenke^2,4 , Heinz-Joachim-Radzun¹ , Walter Stühmer² and Luis A Pardo^2,4

¹Department of Pathology, Georg-August University, Robert-Koch-Str. 40, 37075 Göttingen, Germany

²Max-Planck Institute of Experimental Medicine, Hermann-Rein-Str. 3, 37075 Göttingen, Germany

³Divisão de Farmacologia, Coordenação de Pesquisa, Instituto Nacional do Câncer, Rua André Cavalcanti 37/3° andar, Rio de Janeiro, Brasil

⁴iOnGen AG, Stiegbreite 13, 37077 Göttingen, Germany

⁵DFG Research Center for the Molecular Physiology of the Brain (CMPB), Göttingen, Germany

author email corresponding author email

Molecular Cancer 2006, 5:41doi:10.1186/1476-4598-5-41

Published:	5 October 2006

Abstract

Background

Certain types of potassium channels (known as Eag1, KCNH1, Kv10.1) are associated with the production of tumours in patients and in animals. We have now studied the expression pattern of the Eag1 channel in a large range of normal and tumour tissues from different collections utilising molecular biological and immunohistochemical techniques.

Results

The use of reverse transcription real-time PCR and specifically generated monoclonal anti-Eag1 antibodies showed that expression of the channel is normally limited to specific areas of the brain and to restricted cell populations throughout the body. Tumour samples, however, showed a significant overexpression of the channel with high frequency (up to 80% depending on the tissue source) regardless of the detection method (staining with either one of the antibodies, or detection of Eag1 RNA).

Conclusion

Inhibition of Eag1 expression in tumour cell lines reduced cell proliferation. Eag1 may therefore represent a promising target for the tailored treatment of human tumours. Furthermore, as normal cells expressing Eag1 are either protected by the blood-brain barrier or represent the terminal stage of normal differentiation, Eag1 based therapies could produce only minor side effects.