ReviewCurrent opinion in pharmacology2018
Novel approach to temozolomide resistance in malignant glioma: connexin43-directed therapeutics.
Review in Current opinion in pharmacology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
40 citing papers in PubMed, 67 citations in OpenAlex.
- Actin, connexin-43 and GAP-43 expression in gliomas: real-world associations with IDH status, tumor burden and survival.Journal of neuro-oncology · 2026Article
- Connexin 43 drives glioblastoma cancer stem cell phenotypes through a WNK lysine-deficient protein kinase 1-c-MYC signaling axis.Cell reports · 2025Article
- Association of Hsa_circ_0059511 with the sensitivity of the temozolomide chemotherapeutic treatment in human glioma cells.Scientific reports · 2025Article
- Tonabersat enhances temozolomide-mediated cytotoxicity in glioblastoma by disrupting intercellular connectivity through connexin 43 inhibition.Molecular oncology · 2025Article
- Review
- Neuronal Differentiation of Human Glioma Cells Induced by Parthenolide Under In Vitro Conditions.Biomedicines · 2024Article
- Inhibiting lncRNA NEAT1 Increases Glioblastoma Response to TMZ by Reducing Connexin 43 Expression.Cancer reports (Hoboken, N.J.) · 2024Article
- Chlorpromazine overcomes temozolomide resistance in glioblastoma by inhibiting Cx43 and essential DNA repair pathways.Journal of translational medicine · 2024Article
- Cell Death, by Any Other Name….Cells · 2024Review
- Decreased eukaryotic initiation factors expression upon temozolomide treatment-potential novel implications for eIFs in glioma therapy.Journal of neuro-oncology · 2023Article
- Exosomes-mediated crosstalk between glioma and immune cells in the tumor microenvironment.CNS neuroscience & therapeutics · 2023Review
- αCT1 peptide sensitizes glioma cells to temozolomide in a glioblastoma organoid platform.Biotechnology and bioengineering · 2023Article
- Connexin43 in Musculoskeletal System: New Targets for Development and Disease Progression.Aging and disease · 2022Article
- Review on the Therapeutic Potential of Curcumin and its Derivatives on Glioma Biology.Neurochemical research · 2022Review
- lncRNA XLOC013218 promotes cell proliferation and TMZ resistance by targeting the PIK3R2-mediated PI3K/AKT pathway in glioma.Cancer science · 2022Article
- MiR-493-5p inhibits the malignant development of gliomas via suppressing E2F3-mediated dysfunctions of P53 and PI3K/AKT pathways.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2022Article
- Connexin 43 confers chemoresistance through activating PI3K.Oncogenesis · 2022Article
- Cancer nanotechnology: current status and perspectives.Nano convergence · 2021Review
- The advanced development of Cx43 and GAP-43 mediated intercellular networking in IDH1 wildtype diffuse and anaplastic gliomas with lower mitotic rate.Journal of cancer research and clinical oncology · 2021Article
- Connexin 43 and Sonic Hedgehog Pathway Interplay in Glioblastoma Cell Proliferation and Migration.Biology · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
Abstract
Resistance of malignant glioma, including glioblastoma (GBM), to the chemotherapeutic temozolomide (TMZ) remains a key obstacle in treatment strategies. The gap junction protein connexin43 (Cx43) has complex roles in the establishment, progression, and persistence of malignant glioma. Recent findings demonstrate that connexins play an important role in the microenvironment of malignant glioma and that Cx43 is capable of conferring chemotherapeutic resistance to GBM cells. Carboxyl-terminal Cx43 peptidomimetics show therapeutic promise in overcoming TMZ resistance via mechanisms that may include modulating junctional activity between tumor cells and peritumoral cells and/or downstream molecular signaling events mediated by Cx43 protein binding. High levels of intra-tumor and inter-tumor heterogeneity make it difficult to clearly define specific populations for Cx43-targeted therapy; hence, development of in vitro models that better mimic the microenvironment of malignant glioma, and the incorporation of patient-derived stem cells, could provide opportunities for patient-specific drug screening. This review summarizes recent advances in understanding the roles of Cx43 in malignant glioma, with a special focus on tumor microenvironment, TMZ resistance, and therapeutic opportunity offered by Cx43 peptidomimetics.
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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 OpenQuestion graph.