Evidence map›Paper›PMID 28786347›Full record

ReviewCurrent neuropharmacology2018

KCa3.1 Channels and Glioblastoma: In Vitro Studies.

Lukas Klumpp, Efe C Sezgin, Marco Skardelly, Franziska Eckert, Stephan M Huber

Open access · greenAbstract readReview
In one paragraph

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 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
2.5field-weighted citation impact, top 10% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

38 citing papers in PubMed, 65 citations in OpenAlex.

  1. KCa3.1 mediates radioresistance of silver nanoparticles in human glioblastoma cells.Pflugers Archiv : European journal of physiology · 2026
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  7. Piezo1, the new actor in cell volume regulation.Pflugers Archiv : European journal of physiology · 2024
    Review
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  14. IKCell death & disease · 2022
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  17. Ion Transport and Radioresistance.Reviews of physiology, biochemistry and pharmacology · 2022
    Review
  18. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Lukas KlumppDepartment of Radiation Oncology, University of Tubingen, Tubingen, Germany.
Efe C SezginDepartment of Radiation Oncology, University of Tubingen, Tubingen, Germany.
Marco SkardellyDepartment of Neurosurgery, University of Tubingen, Tubingen, Germany.
Franziska EckertDepartment of Radiation Oncology, University of Tubingen, Tubingen, Germany.
Stephan M HuberDepartment of Radiation Oncology, University of Tubingen, Tubingen, Germany.
University of Tübingen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSeveral tumor entities including brain tumors aberrantly overexpress intermediate conductance Ca2+ activated KCa3.1 K+ channels. These channels contribute significantly to the transformed phenotype of the tumor cells.

methodPubMed was searched in order to summarize our current knowledge on the molecular signaling upstream and downstream and the effector functions of KCa3.1 channel activity in tumor cells in general and in glioblastoma cells in particular. In addition, KCa3.1 expression and function for repair of DNA double strand breaks was determined experimentally in primary glioblastoma cultures in dependence on the abundance of proneural and mesenchymal stem cell markers.

resultsBy modulating membrane potential, cell volume, Ca2+ signals and the respiratory chain, KCa3.1 channels in both, plasma and inner mitochondrial membrane, have been demonstrated to regulate many cellular processes such as migration and tissue invasion, metastasis, cell cycle progression, oxygen consumption and metabolism, DNA damage response and cell death of cancer cells. Moreover, KCa3.1 channels have been shown to crucially contribute to resistance against radiotherapy. Futhermore, the original in vitro data on KCa3.1 channel expression in subtypes of glioblastoma stem(-like) cells propose KCa3.1 as marker for the mesenchymal subgroup of cancer stem cells and suggest that KCa3.1 contributes to the therapy resistance of mesenchymal glioblastoma stem cells.

conclusionThe data suggest KCa3.1 channel targeting in combination with radiotherapy as promising new tool to eradicate therapy-resistant mesenchymal glioblastoma stem cells.

Indexed as

In Vitro TechniquesAnimalsBrain NeoplasmsCalcium SignalingCell CycleGlioblastomaHumansIntermediate-Conductance Calcium-Activated Potassium ChannelsMembrane PotentialsPubMedTumor Cells, CulturedUp-RegulationIntermediate-Conductance Calcium-Activated Potassium ChannelsKCNN4 protein, humanALDH1A3GBMGSCsIKCaKCNN4radioresistanceSK4γH2AX foci.

Identifiers

PMID28786347
PMCPMC5997865
OpenAlexW2745299804

What OpenQuestion holds

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Registered trials

None linked

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.