Eag1 expression interferes with hypoxia homeostasis and induces angiogenesis in 
tumors

Downie, B. R.; Sanchez, A.; Knotgen, H.; Contreras-Jurado, C.; Gymnopoulos, M.; Weber, C.; Stuhmer, W.; Pardo, L. A.

doi:10.1074/jbc.M801830200

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Journal Article

Eag1 expression interferes with hypoxia homeostasis and induces angiogenesis in tumors

MPS-Authors

Downie, B. R.
Max Planck Society;

Sanchez, A.
Max Planck Society;

Knotgen, H.
Max Planck Society;

Contreras-Jurado, C.
Max Planck Society;

Gymnopoulos, M.
Max Planck Society;

Weber, C.
Max Planck Society;

Stuhmer, W.
Max Planck Society;

Pardo, L. A.
Max Planck Society;

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https://www.ncbi.nlm.nih.gov/pubmed/18927085
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Citation

Downie, B. R., Sanchez, A., Knotgen, H., Contreras-Jurado, C., Gymnopoulos, M., Weber, C., et al. (2008). Eag1 expression interferes with hypoxia homeostasis and induces angiogenesis in tumors. J Biol Chem, 283(52), 36234-40. doi:10.1074/jbc.M801830200.

Cite as: https://hdl.handle.net/21.11116/0000-0009-F227-A

Abstract

Ether-a-go-go-1 (Eag1) is a CNS-localized voltage-gated potassium channel that is found ectopically expressed in a majority of extracranial solid tumors. While circumstantial evidence linking Eag1 to tumor biology has been well established, the mechanisms by which the channel contributes to tumor progression remain elusive. In this study, we have used in vivo and in vitro techniques to identify a candidate mechanism. A mutation that eliminates ion permeation fails to completely abolish xenograft tumor formation by transfected cells, indicating that Eag1 contributes to tumor progression independently of its primary function as an ion channel. Our data suggest that Eag1 interferes with the cellular mechanism for maintaining oxygen homeostasis, increasing HIF-1 activity, and thereby VEGF secretion and tumor vascularization.