Ion channels, specifically those controlling the flux of potassium across cell membranes, have recently been shown to exhibit an important role in the pathophysiology of glioma, the most common primary central nervous system tumor with a poor prognosis. Potassium channels are grouped into four subfamilies differing by their domain structure, gating mechanisms, and functions. Pertinent literature indicates the vital functions of potassium channels in many aspects of glioma carcinogenesis, including proliferation, migration, and apoptosis. The dysfunction of potassium channels can result in pro-proliferative signals that are highly related to calcium signaling as well. Moreover, this dysfunction can feed into migration and metastasis, most likely by increasing the osmotic pressure of cells allowing the cells to initiate the "escape" and "invasion" of capillaries. Reducing the expression or channel blockage has shown efficacy in reducing the proliferation and infiltration of glioma cells as well as inducing apoptosis, priming several approaches to target potassium channels in gliomas pharmacologically. This review summarizes the current knowledge on potassium channels, their contribution to oncogenic transformations in glioma, and the existing perspectives on utilizing them as potential targets for therapy.
Keywords: apoptosis; drug repurposing; glioma; migration; potassium channel inhibitors; potassium channels; proliferation.