ArticleCell communication and signaling : CCS2025
Connexin hemichannel blockade by abEC1.1 disrupts glioblastoma progression, suppresses invasiveness, and reduces hyperexcitability in preclinical models.
Article in Cell communication and signaling : CCS, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Astrocytes in neuroinflammation and brain cancer.Molecular biomedicine · 2026Review
- Structure-based virtual screening for selective connexin hemichannel blockers: a historical perspective on the discovery of a small organic inhibitor.Frontiers in pharmacology · 2026Article
- Beyond synapses non-synaptic neural microenvironment interactions remodel circuits and drive glioma progression.Frontiers in oncology · 2026Review
- Modeling gliomas with organoids: reconstructing the human neural microenvironment for translational neuro-oncology.Frontiers in oncology · 2026Review
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Authors and funding
18 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundConnexin (Cx) hemichannels (HCs) contribute to glioblastoma (GBM) progression by facilitating intercellular communication and releasing pro-tumorigenic molecules, including ATP and glutamate.
methodsThe efficacy of abEC1.1, a monoclonal antibody that inhibits Cx26, Cx30, and Cx32 HCs, was assessed in vitro by measuring invasion capability, dye and Ca
resultsabEC1.1 suppressed GBM cell invasion, reducing gliotransmitter release, and impairing tumor progression. In patient-derived GBM cultures, abEC1.1 significantly decreased cell migration and ATP/glutamate release. In vivo, AAV-mediated antibody gene delivery or CED of the purified antibody reduced tumor burden and prolonged survival in the GL261 syngeneic mouse model of GBM. Furthermore, abEC1.1 mitigated glioma-induced excitatory synaptic activity in the 2D co-culture model, suggesting a dual role in tumor control and hyperexcitability suppression.
conclusionsOur findings establish Cx HC inhibition as a promising therapeutic avenue in GBM and highlight abEC1.1 as a potential candidate for clinical translation.
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Registered trials
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 Socratic graph.