Ion channels in glioblastoma

Abstract

Glioblastoma is the most common primary brain tumor with the most dismal prognosis. It is characterized by extensive invasion, migration, and angiogenesis. Median survival is only 15 months due to this behavior, rendering focal surgical resection ineffective and adequate radiotherapy impossible. At this moment, several ion channels have been implicated in glioblastoma proliferation, migration, and invasion. This paper summarizes studies on potassium, sodium, chloride, and calcium channels of glioblastoma. It provides an up-to-date overview of the literature that could ultimately lead to new therapeutic targets.

Figure 1

gBK channels (a) facilitate an increased outwardly K⁺ current. Ca²⁺ input for gBK channels is provided by IP₃R (b). ClC-3 channels facilitate an increased Cl⁻ outwardly current. (a) and (c) facilitate increased H₂O movement through osmosis (d) over the plasma membrane. Glioblastoma AMPA receptors (e) lack the GluR2 subunit and therefore have increased Ca²⁺ permeability. Amiloride-sensitive BNaC channels (f) are expressed in glioblastoma. K_ir channels are mislocalized to the cell nucleus (g), diminishing inwardly rectifying K⁺ currents.