ArticlePloS one2012
The inhibition of KCa3.1 channels activity reduces cell motility in glioblastoma derived cancer stem cells.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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Who cites it
50 citing papers in PubMed, 81 citations in OpenAlex.
- Ion Channel-Targeting Modulators in Glioma: Pharmacological Advances and Therapeutic Perspectives.International journal of molecular sciences · 2026Review
- Co-targeting CDK4/6 and MEK reverses mesenchymal transition in therapy-refractory BRAF-altered pediatric high-grade glioma.Journal of experimental & clinical cancer research : CR · 2026Article
- Deciphering the Role of Functional Ion Channels in Cancer Stem Cells (CSCs) and Their Therapeutic Implications.International journal of molecular sciences · 2025Review
- Computational engineering of water-soluble human potassium ion channels through QTY transformation.Scientific reports · 2024Article
- Piezo1, the new actor in cell volume regulation.Pflugers Archiv : European journal of physiology · 2024Review
- Electrophysiological Impact of SARS-CoV-2 Envelope Protein in U251 Human Glioblastoma Cells: Possible Implications in Gliomagenesis?International journal of molecular sciences · 2024Article
- Challenges in the Therapeutic Targeting of KCa Channels: From Basic Physiology to Clinical Applications.International journal of molecular sciences · 2024Review
- Efficacy of combined tumor irradiation and KScientific reports · 2023Article
- Potassium Ion Channels in Glioma: From Basic Knowledge into Therapeutic Applications.Membranes · 2023Review
- Aggressive migration in acidic pH of a glioblastoma cancer stem cell line in vitro is independent of ASIC and KPflugers Archiv : European journal of physiology · 2023Article
- Insights into the mechanisms governing P01 scorpion toxin effect against U87 glioblastoma cells oncogenesis.Frontiers in pharmacology · 2023Article
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- Ion Channel Drugs Suppress Cancer Phenotype in NG108-15 and U87 Cells: Toward Novel Electroceuticals for Glioblastoma.Cancers · 2022Article
- Potassium Channels as a Target for Cancer Therapy: Current Perspectives.OncoTargets and therapy · 2022Review
- Ion Transport and Radioresistance.Reviews of physiology, biochemistry and pharmacology · 2022Review
- Chimeric Stimuli-Responsive Liposomes as Nanocarriers for the Delivery of the Anti-Glioma Agent TRAM-34.International journal of molecular sciences · 2021Article
- Identification of candidate genes associated with papillary thyroid carcinoma pathogenesis and progression by weighted gene co-expression network analysis.Translational cancer research · 2021Article
- Deciphering the Role of CaCancers · 2021Review
- Ion Channels in Glioma Malignancy.Reviews of physiology, biochemistry and pharmacology · 2021Review
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In the present study we evaluated the expression of the intermediate conductance calcium-activated potassium (KCa3.1) channel in human glioblastoma stem-like cells (CSCs) and investigated its role in cell motility. While the KCa3.1 channel is not expressed in neuronal- and glial-derived tissues of healthy individuals, both the KCa3.1 mRNA and protein are present in the glioblastoma tumor population, and are significantly enhanced in CSCs derived from both established cell line U87MG and a primary cell line, FCN9. Consistent with these data, voltage-independent and TRAM-34 sensitive potassium currents imputable to the KCa3.1 channel were recorded in the murine GL261 cell line and several primary human glioblastoma cells lines. Moreover, a significantly higher KCa3.1 current was recorded in U87MG-CD133 positive cells as compared to the U87MG-CD133 negative subpopulation. Further, we found that the tumor cell motility is strongly associated with KCa3.1 channel expression. Blockade of the KCa3.1 channel with the specific inhibitor TRAM-34 has in fact a greater impact on the motility of CSCs (reduction of 75%), which express a high level of KCa3.1 channel, than on the FCN9 parental population (reduction of 32%), where the KCa3.1 channel is expressed at lower level. Similar results were also observed with the CSCs derived from U87MG. Because invasion of surrounding tissues is one of the main causes of treatment failure in glioblastoma, these findings can be relevant for future development of novel cancer therapeutic drugs.
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