ArticleCancer reports (Hoboken, N.J.)2024
Inhibiting lncRNA NEAT1 Increases Glioblastoma Response to TMZ by Reducing Connexin 43 Expression.
Article in Cancer reports (Hoboken, N.J.), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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.
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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
4 citing papers in PubMed.
- The Role of LncRNAs in Radio- and Chemoresistance of Glioblastoma: Prognostic or Therapeutic?Current oncology (Toronto, Ont.) · 2025Review
- Molecular Interplay Between Non-Coding RNAs and Connexins and Its Possible Role in Cancer.International journal of molecular sciences · 2025Review
- Long Non-Coding RNAs in Malignant Human Brain Tumors: Driving Forces Behind Progression and Therapy.International journal of molecular sciences · 2025Review
- Bibliometric analysis and visualization of Connexin 43 in the field of solid tumor research(2000-2024).Frontiers in immunology · 2025Article
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
objectivesGlioblastoma multiforme (GBM) is considered the most assailant subtype of gliomas, presenting a formidable obstacle because of its inherent resistance to temozolomide (TMZ). This study aimed to characterize the function of lncRNA NEAT1 in facilitating the advancement of gliomas.
methodsThe expression level of NEAT1 in glioma tissues and cells was detected by qRT-PCR. RNA interference experiment, cell proliferation assay, FITC/PI detection assay, immunoblotting, bioinformatics prediction, a double luciferase reporter gene assay, RNA immunoprecipitation (RIP) assay, SLDT assay and correlation analysis of clinical samples were performed to explore the regulatory effects of NEAT1, miR-454-3p and Cx43 and their role in malignant progression of GBM. The role of NEAT1 in vivo was investigated by an intracranial tumor formation experiment in mice.
resultsThe results showed that recurring gliomas displayed elevated levels of NEAT1 compared to primary gliomas. The suppression of NEAT1 led to a restoration of sensitivity in GBM cells to TMZ. NEAT1 functioned as a competitive endogenous RNA against miR-454-3p. Connexin 43 was identified as a miR-454-3p target. NEAT1 was found to regulate gap junctional intercellular communication by modulating Connexin 43, thereby impacting the response of GBM cells to TMZ chemotherapy. Downregulation of NEAT1 resulted in enhanced chemosensitivity to TMZ and extended the survival of mice.
conclusionsOverall, these results indicated that the NEAT1/miR-454-3p/Connexin 43 pathway influences GBM cell response to TMZ and could offer a potential new strategy for treating GBM.
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Registered trials
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