ReviewCurrent neuropharmacology2018
Functional Roles of the Ca2+-activated K+ Channel, KCa3.1, in Brain Tumors.
Review in Current neuropharmacology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 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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Who cites it
14 citing papers in PubMed, 28 citations in OpenAlex.
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- A machine learning-derived angiogenesis signature for clinical prognosis and immunotherapy guidance in colon adenocarcinoma.Scientific reports · 2025Article
- Potassium Ion Channels in Glioma: From Basic Knowledge into Therapeutic Applications.Membranes · 2023Review
- CRAC and SK Channels: Their Molecular Mechanisms Associated with Cancer Cell Development.Cancers · 2022Review
- Astrocytes-Derived Small Extracellular Vesicles Hinder Glioma Growth.Biomedicines · 2022Article
- ATP-evoked intracellular CaJournal of neuroinflammation · 2021Article
- Comparison of KHandbook of experimental pharmacology · 2021Article
- Deeper and Deeper on the Role of BK and Kir4.1 Channels in Glioblastoma Invasiveness: A Novel Summative Mechanism?Frontiers in neuroscience · 2020Review
- Article
- Cancer-Associated Intermediate Conductance CaCancers · 2019Review
- Dexamethasone in Glioblastoma Multiforme Therapy: Mechanisms and Controversies.Frontiers in molecular neuroscience · 2019Review
- CaBrain, behavior, and immunity · 2018Article
- KCa3.1 Channels and Glioblastoma: In Vitro Studies.Current neuropharmacology · 2018Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundGlioblastoma is the most aggressive and deadly brain tumor, with low disease-free period even after surgery and combined radio and chemotherapies. Among the factors contributing to the devastating effect of this tumor in the brain are the elevated proliferation and invasion rate, and the ability to induce a local immunosuppressive environment. The intermediateconductance Ca2+-activated K+ channel KCa3.1 is expressed in glioblastoma cells and in tumorinfiltrating cells.
methodsWe first describe the researches related to the role of KCa3.1 channels in the invasion of brain tumor cells and the regulation of cell cycle. In the second part we review the involvement of KCa3.1 channel in tumor-associated microglia cell behaviour.
resultsIn tumor cells, the functional expression of KCa3.1 channels is important to substain cell invasion and proliferation. In tumor infiltrating cells, KCa3.1 channel activity is required to regulate their activation state. Interfering with KCa3.1 activity can be an adjuvant therapeutic approach in addition to classic chemotherapy and radiotherapy, to counteract tumor growth and prolong patient's survival.
conclusionIn this mini-review we discuss the evidence of the functional roles of KCa3.1 channels in glioblastoma biology.
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