ArticleAmerican journal of cancer research2021
Cilostazol eliminates radiation-resistant glioblastoma by re-evoking big conductance calcium-activated potassium channel activity.
Article in American journal of cancer research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 5 papers.
What it found
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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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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
5 citing papers in PubMed, 8 citations in OpenAlex.
- Ion Channel-Targeting Modulators in Glioma: Pharmacological Advances and Therapeutic Perspectives.International journal of molecular sciences · 2026Review
- Design, Synthesis, and Computational Evaluation of 3,4-Dihydroquinolin-2(Pharmaceuticals (Basel, Switzerland) · 2025Article
- Article
- CXCR7 activation evokes the anti-PD-L1 antibody against glioblastoma by remodeling CXCL12-mediated immunity.Cell death & disease · 2024Article
- Disulfiram Sensitizes a Therapeutic-Resistant Glioblastoma to the TGF-β Receptor Inhibitor.International journal of molecular sciences · 2021Article
Corrections and comments
- Erratum issued
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In spite of radio- and chemotherapy, glioblastoma (GBM) develops therapeutic resistance leading to recurrence and poor prognosis. Therefore, understanding the underlying mechanisms of resistance is important to improve the treatment of GBM. To this end, we developed a radiation-resistant cell model by exposure to consecutive periods of irradiation. Simultaneously, single high-dose irradiation was introduced to determine "when" GBM developed consecutive irradiation-induced resistance (CIIR). We found that CIIR promoted TGF-β secretion, activated pro-survival Akt, and downregulated p21 in a p53-independent manner. Furthermore, CIIR upregulated multidrug-resistant proteins, resulting in temozolomide resistance. CIIR GBM also enhanced cell mobility and accelerated cell proliferation. The big-conductance calcium-activated potassium channel (BK channel) is highly expressed and activated in GBM. However, CIIR diminishes BK channel activity in an expression-independent manner. Cilostazol is a phosphodiesterase-3 inhibitor for the treatment of intermittent claudication and was able to reverse CIIR-induced BK channel inactivation. Paxilline, a BK channel blocker, promoted cell migration and proliferation in parental GBM cells. In contrast, Cilostazol inhibited CIIR-induced cell motility, proliferation, and the ability to form tumor spheres. Moreover, we established a radiation-resistant GBM
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Identifiers
33948351PMC8085866W4287544613What OpenQuestion holds
Registered trials
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