PubMed 18927085
Referenced in: none
Automatically associated channels: Kv10.1
Title: Eag1 expression interferes with hypoxia homeostasis and induces angiogenesis in tumors.
Authors: Bryan R Downie, Araceli Sánchez, Hendrik Knötgen, Constanza Contreras-Jurado, Marco Gymnopoulos, Claudia Weber, Walter Stühmer, Luis A Pardo
Journal, date & volume: J. Biol. Chem., 2008 Dec 26 , 283, 36234-40
PubMed link: http://www.ncbi.nlm.nih.gov/pubmed/18927085
Abstract
Ether-á-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.