ArticleCell reports2025
Connexin 43 drives glioblastoma cancer stem cell phenotypes through a WNK lysine-deficient protein kinase 1-c-MYC signaling axis.
Article in Cell reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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.
The trial behind it
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
9 citing papers in PubMed.
- IsoformSwitchAnalyzeR v2: analysis of functional isoform changes in long-read and single-cell sequencing data.NAR genomics and bioinformatics · 2026Article
- Beyond the gap: moonlighting functions of connexins in cancer.Cell communication and signaling : CCS · 2026Review
- Role of Connexin-43: from cancer initiation to cancer metastasis.Molecular biology reports · 2026Review
- Targeting EHMT2 inhibition in glioblastoma: effects on tumor progression and STAT3 signaling.Translational cancer research · 2026Article
- Hypoxia Increases Connexin46 and Connexin43 Levels in KNS-42 Glioblastoma Cells.International journal of molecular sciences · 2026Article
- Tumor microenvironment shapes the spatial organization of glioblastoma cell states.Neuro-oncology · 2026Review
- Connexin-Pannexin duality in glioblastoma.Cell and tissue research · 2026Review
- A New Predictor Score for Postoperative Seizures in Brain Tumor Patients Without a Seizure History (BRAINNN Score).Cureus · 2025Article
- Connexin-43 in Cancer: Above and Beyond Gap Junctions!Cancers · 2024Review
Corrections and comments
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Authors and funding
14 authors.
Funding
Abstract
The coordination of cellular processes such as growth and survival relies on communication between cells through gap junctions. Connexin proteins comprise gap junctions and also function to mediate protein-protein interactions and communication with the extracellular space via hemichannels. Despite their essential roles, connexin function in cancer is context dependent, with connexin 43 (Cx43) reported to both promote and suppress tumor growth in glioblastoma, the most common primary malignant brain tumor. Here, we detect primarily intracellular expression of Cx43 in glioblastoma patient-derived cancer stem cells and demonstrate that Cx43 is essential for their survival, self-renewal, and tumor initiation. Mechanistically, Cx43 depletion reduces c-MYC expression through reduced levels of the upstream mediator WNK lysine-deficient protein kinase 1 (WNK1). WNK1 depletion phenocopies Cx43 knockdown and reduces c-MYC expression and tumor initiation. Together, these results define a signaling axis downstream of Cx43 that promotes tumor growth and cancer stem cell phenotypes in glioblastoma.
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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.