ArticleCell death & disease2013
KCa3.1 channels are involved in the infiltrative behavior of glioblastoma in vivo.
Article in Cell death & disease, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 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.
The trial behind it
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
87 citing papers in PubMed, 122 citations in OpenAlex.
- Ion Channel-Targeting Modulators in Glioma: Pharmacological Advances and Therapeutic Perspectives.International journal of molecular sciences · 2026Review
- KCa3.1 mediates radioresistance of silver nanoparticles in human glioblastoma cells.Pflugers Archiv : European journal of physiology · 2026Article
- Astrocyte-derived miR-124 impairs glioma cell volume regulation and migration by reducing CaCellular and molecular life sciences : CMLS · 2026Article
- Pro-tumoral CaScientific reports · 2026Article
- A Prognostic Neuromodulation-Related Gene Signature Identifies Immunomodulation and Tumour-Associated Hallmarks in Glioblastoma.Biomedicines · 2025Article
- KCa3.1 channels regulate the tumor infiltration of functionally competent NK cells in head and neck cancer.Scientific reports · 2025Article
- Metal Ion Signaling in Biomedicine.Chemical reviews · 2025Review
- Piezo1, the new actor in cell volume regulation.Pflugers Archiv : European journal of physiology · 2024Review
- Repurposing the KTranslational stroke research · 2024Article
- KCNK1 promotes proliferation and metastasis of breast cancer cells by activating lactate dehydrogenase A (LDHA) and up-regulating H3K18 lactylation.PLoS biology · 2024Article
- Microglia in Glioma.Advances in neurobiology · 2024Review
- Pan-cancer ion transport signature reveals functional regulators of glioblastoma aggression.The EMBO journal · 2024Article
- Neurooncology: 2024 update.Free neuropathology · 2024Article
- Hypoxia, Ion Channels and Glioblastoma Malignancy.Biomolecules · 2023Review
- Efficacy of combined tumor irradiation and KScientific reports · 2023Article
- Review
- 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 Peritumoural Brain Zone of Glioblastoma:International journal of molecular sciences · 2023Article
- Aquaporins and Ion Channels as Dual Targets in the Design of Novel Glioblastoma Therapeutics to Limit Invasiveness.Cancers · 2023Review
27 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 5 institutions in 2 countries.
Funding
Abstract
Glioblastoma multiforme (GBM) is a diffuse brain tumor characterized by high infiltration in the brain parenchyma rendering the tumor difficult to eradicate by neurosurgery. Efforts to identify molecular targets involved in the invasive behavior of GBM suggested ion channel inhibition as a promising therapeutic approach. To determine if the Ca(2+)-dependent K(+) channel KCa3.1 could represent a key element for GBM brain infiltration, human GL-15 cells were xenografted into the brain of SCID mice that were then treated with the specific KCa3.1 blocker TRAM-34 (1-((2-chlorophenyl) (diphenyl)methyl)-1H-pyrazole). After 5 weeks of treatment, immunofluorescence analyses of cerebral slices revealed reduced tumor infiltration and astrogliosis surrounding the tumor, compared with untreated mice. Significant reduction of tumor infiltration was also observed in the brain of mice transplanted with KCa3.1-silenced GL-15 cells, indicating a direct effect of TRAM-34 on GBM-expressed KCa3.1 channels. As KCa3.1 channels are also expressed on microglia, we investigated the effects of TRAM-34 on microglia activation in GL-15 transplanted mice and found a reduction of CD68 staining in treated mice. Similar results were observed in vitro where TRAM-34 reduced both phagocytosis and chemotactic activity of primary microglia exposed to GBM-conditioned medium. Taken together, these results indicate that KCa3.1 activity has an important role in GBM invasiveness in vivo and that its inhibition directly affects glioma cell migration and reduces astrocytosis and microglia activation in response to tumor-released factors. KCa3.1 channel inhibition therefore constitutes a potential novel therapeutic approach to reduce GBM spreading into the surrounding tissue.
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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.