ReviewFrontiers in cellular neuroscience2015
Reconciling the discrepancies on the involvement of large-conductance Ca(2+)-activated K channels in glioblastoma cell migration.
Review in Frontiers in cellular neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
18 citing papers in PubMed, 25 citations in OpenAlex.
- BKJournal of neuro-oncology · 2026Article
- Dibenzoylmethane, a novel β-diketone pore blocker of large-conductance calcium-activated potassium channel.bioRxiv : the preprint server for biology · 2026Article
- Targeting Ion Channels: Blockers Suppress Calcium Signals and Induce Cytotoxicity Across Medulloblastoma Cell Models.Bioengineering (Basel, Switzerland) · 2025Article
- Challenges in the Therapeutic Targeting of KCa Channels: From Basic Physiology to Clinical Applications.International journal of molecular sciences · 2024Review
- Hypoxia, Ion Channels and Glioblastoma Malignancy.Biomolecules · 2023Review
- Role of NaInternational journal of molecular sciences · 2023Article
- Co-dependent regulation of p-BRAF and potassium channel KCNMA1 levels drives glioma progression.Cellular and molecular life sciences : CMLS · 2023Article
- ThemicroPublication biology · 2021Article
- Ion Channels in Glioma Malignancy.Reviews of physiology, biochemistry and pharmacology · 2021Review
- BK Channel-Mediated Microglial Phagocytosis Alleviates Neurological Deficit After Ischemic Stroke.Frontiers in cellular neuroscience · 2021Article
- Squaring the Circle: A New Study of Inward and Outward-Rectifying Potassium Currents in U251 GBM Cells.Cellular and molecular neurobiology · 2020Article
- Deeper and Deeper on the Role of BK and Kir4.1 Channels in Glioblastoma Invasiveness: A Novel Summative Mechanism?Frontiers in neuroscience · 2020Review
- Hyperplasia suppressor gene inhibits the proliferation and metastasis of glioma cells by targeting rho family proteins.International journal of clinical and experimental pathology · 2020Article
- Alternating Electric Fields (TTFields) Activate CaCancers · 2019Article
- Cancer-Associated Intermediate Conductance CaCancers · 2019Review
- Dexamethasone in Glioblastoma Multiforme Therapy: Mechanisms and Controversies.Frontiers in molecular neuroscience · 2019Review
- BK channels blockage inhibits hypoxia-induced migration and chemoresistance to cisplatin in human glioblastoma cells.Journal of cellular physiology · 2018Article
- Calcium-gated KPflugers Archiv : European journal of physiology · 2017Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glioblastoma (GBM) is the most common and aggressive primary brain tumor, and is notable for spreading so effectively through the brain parenchyma to make complete surgical resection virtually impossible, and prospect of life dismal. Several ion channels have been involved in GBM migration and invasion, due to their critical role in supporting volume changes and Ca(2+) influx occuring during the process. The large-conductance, Ca(2+)-activated K (BK) channels, markedly overexpressed in biopsies of patients with GBMs and in GBM cell lines, have attracted much interest and have been suggested to play a central role in cell migration and invasion as candidate channels for providing the ion efflux and consequent water extrusion that allow cell shrinkage during migration. Available experimental data on the role of BK channel in migration and invasion are not consistent though. While BK channels block typically resulted in inhibition of cell migration or in no effect, their activation would either enhance or inhibit the process. This short review reexamines the relevant available data on the topic, and presents a unifying paradigm capable of reconciling present discrepancies. According to this paradigm, BK channels would not contribute to migration under conditions where the [Ca(2+)] i is too low for their activation. They will instead positively contribute to migration for intermediate [Ca(2+)] i , insufficient as such to activate BK channels, but capable of predisposing them to cyclic activation following oscillatory [Ca(2+)] i increases. Finally, steadily active BK channels because of prolonged high [Ca(2+)] i would inhibit migration as their steady activity would be unsuitable to match the cyclic cell volume changes needed for proper cell migration.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.