Review uncovers rising evidence of calcium-activated potassium channels' role in glioblastoma, suggesting innovative therapies to combat tumor resistance.
Potassium channels in brain tissue orchestrate essential cellular processes, including the regulation of membrane potential and neuronal excitability. Among them, large‐conductance calcium‐activated potassium (BK Ca ) channels play a pivotal role in both normal brain physiology and the pathogenesis of glioblastoma multiforme, a highly aggressive primary brain tumor. Within the central nervous system, BK Ca channels are widely expressed in neurons, astrocytes, and oligodendrocytes, contributing to ion homeostasis and synaptic transmission. In glioblastoma cells, overexpression of BK Ca channels, particularly the glioma‐specific gBK Ca variant, facilitates tumor progression by enhancing cell migration, invasion, and therapeutic resistance. Recent evidence highlights the significance of the mitochondrial isoform of the BK Ca channel (mitoBK Ca ) in modulating oxidative phosphorylation and reactive oxygen species generation, thereby promoting tumor cell survival under hypoxic and cytotoxic stress. This review summarizes current insights into the role of BK Ca and mitoBK Ca channels in glioblastoma biology, their potential classification as oncochannels, and the emerging pharmacological strategies targeting these channels, emphasizing the translational challenges in developing BK Ca ‐directed therapies for glioblastoma treatment.
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Jaworowska et al. (2025) studied this question.
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