ReviewFrontiers in neuroscience2020
Deeper and Deeper on the Role of BK and Kir4.1 Channels in Glioblastoma Invasiveness: A Novel Summative Mechanism?
Review in Frontiers in neuroscience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 26 citations in OpenAlex.
- Potential therapeutic targeting of BKMolecular oncology · 2026Review
- The progression of triple-negative breast cancer is linked to a gradual decrease of the BK channel in the plasma membrane and an increase in intracellular structures.Pflugers Archiv : European journal of physiology · 2026Article
- A Machine Learning-Driven Electrophysiological Platform for Real-Time Tumor-Neural Interaction Analysis and Modulation.Nature communications · 2026Article
- Druggability of Sodium Calcium Exchanger (NCX): Challenges and Recent Development.International journal of molecular sciences · 2025Review
- Review
- Functional expression of the proton sensors ASIC1a, TMEM206, and OGR1 together with BKPflugers Archiv : European journal of physiology · 2024Article
- Ion Channels and Ionotropic Receptors in Astrocytes: Physiological Functions and Alterations in Alzheimer's Disease and Glioblastoma.Life (Basel, Switzerland) · 2023Review
- Three-Dimensional Gene Regulation Network in Glioblastoma Ferroptosis.International journal of molecular sciences · 2023Article
- Role of NaInternational journal of molecular sciences · 2023Article
- Article
- Remote neuronal activity drives glioma infiltration via Sema4f.bioRxiv : the preprint server for biology · 2023Article
- CaInternational journal of molecular sciences · 2023Review
- Review
- New Potential Agents for Malignant Melanoma Treatment-Most Recent Studies 2020-2022.International journal of molecular sciences · 2022Review
- Ion Channel Drugs Suppress Cancer Phenotype in NG108-15 and U87 Cells: Toward Novel Electroceuticals for Glioblastoma.Cancers · 2022Article
- Tumor Cell Infiltration into the Brain in Glioblastoma: From Mechanisms to Clinical Perspectives.Cancers · 2022Review
- Homology modeling and molecular docking simulation of martentoxin as a specific inhibitor of the BK channel.Annals of translational medicine · 2022Article
- Transcriptome profiles of fatty acid metabolism-related genes and immune infiltrates identify hot tumors for immunotherapy in cutaneous melanoma.Frontiers in genetics · 2022Article
- Bioactive peptides from venoms against glioma progression.Frontiers in oncology · 2022Review
- Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In the last decades, increasing evidence has revealed that a large number of channel protein and ion pumps exhibit impaired expression in cancers. This dysregulation is responsible for high proliferative rates as well as migration and invasiveness, reflected in the recently coined term oncochannelopathies. In glioblastoma (GBM), the most invasive and aggressive primary brain tumor, GBM cells modify their ionic equilibrium in order to change their volume as a necessary step prior to migration. This mechanism involves increased expression of BK channels and downregulation of the normally widespread Kir4.1 channels, as noted in GBM biopsies from patients. Despite a large body of work implicating BK channels in migration in response to an artificial intracellular calcium rise, little is known about how this channel acts in GBM cells at resting membrane potential (RMP), as compared to other channels that are constitutively open, such as Kir4.1. In this review we propose that a residual fraction of functionally active Kir4.1 channels mediates a small, but continuous, efflux of potassium at the more depolarized RMP of GBM cells. In addition, coinciding with transient membrane deformation and the intracellular rise in calcium concentration, brief activity of BK channels can induce massive and rapid cytosolic water loss that reduces cell volume (cell shrinkage), a necessary step for migration within the brain parenchyma.
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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.