ArticleCancers2025
KATP Channel Inhibitors Reduce Cell Proliferation Through Upregulation of H3K27ac in Diffuse Intrinsic Pontine Glioma: A Functional Expression Investigation.
Article in Cancers, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Safety and Efficacy of Mosunetuzumab: Experience in the Hospital Cardinale Giovanni Panico.Antibodies (Basel, Switzerland) · 2026Article
- Actions of Midostaurin as Cation Channel and Tyrosine Kinase Inhibitor in Diffuse Intrinsic Pontine Glioma Cell Lines.Cancers · 2026Article
- Targeting ion channel dysregulation in tumors: emerging therapeutic opportunities.Trends in pharmacological sciences · 2026Review
- Dysregulation of human ClpP using small molecules with piperazine-based scaffold for diffuse intrinsic pontine glioma therapy validated by patient-derived tumor organoids.Research square · 2026Article
- Decoding Gene Expression Changes in Cerebral Tumors: Before and After Radiotherapy.Medicinal research reviews · 2025Review
- Mitochondrial Protease ClpP: Cancer Marker and Drug Target.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Review
- Can Focused Ultrasound Overcome the Failure of Chemotherapy in Treating Pediatric Diffuse Intrinsic Pontine Glioma Due to a Blood-Brain Barrier Obstacle?Pharmaceuticals (Basel, Switzerland) · 2025Review
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundDiffuse intrinsic pontine glioma [DIPG] is a fatal pediatric disease characterized by a post-translational modification, a replacement of lysine by methionine in position 27 of the N-terminal [H3K27M] tail of histone 3 isoform-1 [H3.1] or histone 3 isoform-3 [H3.3], respectively, expressed in the DIPG-36 and DIPG-50 cells. We investigated the role of cation channels in DIPG cells for the first time and the effects of ATP-sensitive K
methodsExperiments were performed using "in vitro" cytotoxic assays combined with the patch clamp technique, RT-PCR, Western blot, and flow cytometry assays.
resultsThe most effective anti-proliferative drugs were repaglinide and glibenclamide after short and long-term incubation [6-96 h]. These drugs reduced macroscopic currents of the DIPG cells recorded in whole-cell patch clamp. Repaglinide concentration dependently enhanced the target protein H3K27ac in Western blotting after 48 h of incubation. This drug reduced cell diameter and enhanced cleaved caspase-3 in DIPG cells; total AKT/mTOR levels and phospho-mTOR were downregulated in DIPG-36.
conclusionsKATP and TRPV1 channels are functionally expressed, and sulphonylureas are effective antiproliferative upregulating H3K27ac with apoptosis in DIPG cells and the sub-micromolar concentrations in DIPG-50.
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