ArticleOncology letters2016
Suppression of the Eag1 potassium channel sensitizes glioblastoma cells to injury caused by temozolomide.
Article in Oncology letters, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 34 citations in OpenAlex.
- New insights into the physiological, pathological and pharmacological roles of voltage‑gated potassium channel Kv10.1 in cancer (Review).International journal of oncology · 2026Review
- Apoptotic and senolytic effects of hERG/Eag1 channel blockers in combination with temozolomide in human glioblastoma cells.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- A designer peptide against the EAG2-Kvβ2 potassium channel targets the interaction of cancer cells and neurons to treat glioblastoma.Nature cancer · 2023Article
- Potassium Ion Channels in Glioma: From Basic Knowledge into Therapeutic Applications.Membranes · 2023Review
- Review
- Targeting Ion Channels for Cancer Treatment: Current Progress and Future Challenges.Reviews of physiology, biochemistry and pharmacology · 2022Review
- Potassium Channels as a Target for Cancer Therapy: Current Perspectives.OncoTargets and therapy · 2022Review
- Electrotherapies for Glioblastoma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2021Review
- Modifications of Plasma Membrane Organization in Cancer Cells for Targeted Therapy.Molecules (Basel, Switzerland) · 2021Review
- Methadone-mediated sensitization of glioblastoma cells is drug and cell line dependent.Journal of cancer research and clinical oncology · 2021Article
- Potassium Channels in Cancer.Handbook of experimental pharmacology · 2021Article
- Comparison of Elemental Anomalies Following Implantation of Different Cell Lines of Glioblastoma Multiforme in the Rat Brain: A Total Reflection X-ray Fluorescence Spectroscopy Study.ACS chemical neuroscience · 2020Article
- Review
- Drug Repositioning Screen on a New Primary Cell Line Identifies Potent Therapeutics for Glioblastoma.Frontiers in neuroscience · 2020Article
- Voltage-Gated Potassium Channels as Regulators of Cell Death.Frontiers in cell and developmental biology · 2020Review
- Antibodies Targeting KBioelectricity · 2019Article
- Suppressing nNOS Enzyme by Small-Interfering RNAs Protects SH-SY5Y Cells and Nigral Dopaminergic Neurons from 6-OHDA Injury.Neurotoxicity research · 2019Article
- Delivery of miRNA-Targeted Oligonucleotides in the Rat Striatum by Magnetofection with NeuromagMolecules (Basel, Switzerland) · 2018Article
- Function of neuronal nitric oxide synthase enzyme in temozolomide-induced damage of astrocytic tumor cells.Oncology letters · 2018Article
- Astemizole Inhibits mTOR Signaling and Angiogenesis by Blocking Cholesterol Trafficking.International journal of biological sciences · 2018Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glioblastoma multiforme (GBM) is the most aggressive type of human primary brain tumor. The standard treatment protocol includes radiotherapy in combination with temozolomide (TMZ). Despite advances in GBM treatment, the survival time of patients diagnosed with glioma is 14.5 months. Regarding tumor biology, various types of cancer cell overexpress the ether à go-go 1 (Eag1) potassium channel. Therefore, the present study examined the role of Eag1 in the cell damage caused by TMZ on the U87MG glioblastoma cell line. Eag1 was inhibited using a channel blocker (astemizole) or silenced by a short-hairpin RNA expression vector (pKv10.1-3). pKv10.1-3 (0.2 µg) improved the Eag1 silencing caused by 250 µM TMZ, as determined by reverse transcription-quantitative polymerase chain reaction and immunocytochemistry. Additionally, inhibiting Eag1 with the vector or astemizole (5 µM) reduced glioblastoma cell viability and sensitized cells to TMZ. Cell viability decreased by 63% for pKv10.1-3 + TMZ compared with 34% for TMZ alone, and by 77% for astemizole + TMZ compared with 46% for TMZ alone, as determined by MTT assay. In addition, both the vector and astemizole increased the apoptosis rate of glioblastoma cells triggered by TMZ, as determined by an Annexin V apoptosis assay. Collectively, the current data reveal that Eag1 has a role in the damage caused to glioblastoma by TMZ. Furthermore, suppression of this channel can improve the action of TMZ on U87MG glioblastoma cells. Thus, silencing Eag1 is a promising strategy to improve GBM treatment and merits additional studies in animal models of glioma.
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