ArticleBritish journal of pharmacology2012
Inhibition of T-type Ca²⁺ channels by endostatin attenuates human glioblastoma cell proliferation and migration.
Article in British journal of pharmacology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers, 2 of them syntheses that pooled it.
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Who cites it
60 citing papers in PubMed, 2 syntheses or guidelines pooled it, 132 citations in OpenAlex.
- Calcium channelopathies and intellectual disability: a systematic review.Orphanet journal of rare diseases · 2021Pooled it
- Screening key genes and pathways in glioma based on gene set enrichment analysis and meta-analysis.Journal of molecular neuroscience : MN · 2013Pooled it
- Ion Channel-Targeting Modulators in Glioma: Pharmacological Advances and Therapeutic Perspectives.International journal of molecular sciences · 2026Review
- ROS-induced voltage-gated ion channel expression and electrophysiological remodeling in malignant human cells.NPJ systems biology and applications · 2025Article
- Current evidence and challenges of multitarget anti-angiogenic agents for glioblastoma: Results from clinical trials.iScience · 2025Review
- Biophysical Properties of Somatic Cancer Mutations in the S4 Transmembrane Segment of the Human Voltage-Gated Proton Channel hHBiomolecules · 2025Article
- Novel insights into voltage-gated ion channels: Translational breakthroughs in medical oncology.Channels (Austin, Tex.) · 2024Article
- CACNA1H restrains chemotherapy resistance in ovarian clear cell carcinoma cells by repressing autophagy.Molecular genetics and genomics : MGG · 2024Article
- Obesity and Depression: Common Link and Possible Targets.CNS & neurological disorders drug targets · 2024Review
- Integrated profiling identifies CACNG3 as a prognostic biomarker for patients with glioma.BMC cancer · 2023Article
- Adiponectin receptor 1-mediated stimulation of Cav3.2 channels in trigeminal ganglion neurons induces nociceptive behaviors in mice.The journal of headache and pain · 2023Article
- Trace amine-associated receptor 1 regulation of Kv1.4 channels in trigeminal ganglion neurons contributes to nociceptive behaviors.The journal of headache and pain · 2023Article
- Article
- The peritumoral brain zone in glioblastoma: where we are and where we are going.Journal of neuroscience research · 2023Review
- Inactivation of CACNA1H induces cell apoptosis by initiating endoplasmic reticulum stress in glioma.Translational neuroscience · 2023Article
- Calcium and activity-dependent signaling in the developing cerebral cortex.Development (Cambridge, England) · 2022Review
- T-Type Calcium Channel Inhibitors Induce Apoptosis in Medulloblastoma Cells Associated with Altered Metabolic Activity.Molecular neurobiology · 2022Article
- Strengthening Anti-Glioblastoma Effect by Multi-Branched Dendrimers Design of a Scorpion Venom Tetrapeptide.Molecules (Basel, Switzerland) · 2022Article
- Modification of mesenchymal stem cells by HMGB1 promotes the activity of Cav3.2 T-type calcium channel via PKA/β-catenin/γ-cystathionase pathway.Stem cell research & therapy · 2022Article
- The modulation of ion channels in cancer chemo-resistance.Frontiers in oncology · 2022Review
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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
background and purposeEndostatin (ES) is a c-terminal proteolytic fragment of collagen XVIII with promising antitumour properties in several tumour models, including human glioblastoma. We hypothesized that this peptide could interact with plasma membrane ion channels and modulate their functions. EXPERIMENTAL APPROACH: Using cell proliferation and migration assays, patch clamp and Western blot analysis, we studied the effects of ES on the proliferation and migration of human glioblastoma U87 cells, mediated by T-type Ca²⁺ channels. KEY
resultsExtracellular application of ES reversibly inhibited T-type Ca²⁺ channel currents (T-currents) in U87 cells, whereas L-type Ca²⁺ currents were not affected. This inhibitory effect was associated with a hyperpolarizing shift in the voltage-dependence of inactivation but was independent of G-protein and protein tyrosine kinase-mediated pathways. All three α₁ subunits of T-type Ca²⁺ channels (Ca(V) 3), α(1G) (Ca(V) 3.1), α(1H) (Ca(V) 3.2) and α(1I) (Ca(V) 3.3), were endogenously expressed in U87 cells. Using transfected HEK293 or CHO cells, we showed that only Ca(V) 3.1 and Ca(V) 3.2, but not Ca(V) 3.3 or Ca(V) 1.2 (L-type), channel currents were significantly inhibited. More interestingly, ES inhibited the proliferation and migration of U87 cells in a dose-dependent manner. Pretreatment of the cells with the specific T-type Ca²⁺ channel blocker mibefradil occluded these inhibitory effects of ES. CONCLUSION AND IMPLICATIONS: This study provides the first evidence that the antitumour effects of ES on glioblastoma cells is through direct inhibition of T-type Ca²⁺ channels and gives new insights into the future development of a new class of antiglioblastoma agents that target the proliferation and migration of these cells.
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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.