ArticleFrontiers in pharmacology2019
Cycling Quiescence in Temozolomide Resistant Glioblastoma Cells Is Partly Explained by microRNA-93 and -193-Mediated Decrease of Cyclin D.
Article in Frontiers in pharmacology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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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
21 citing papers in PubMed, 26 citations in OpenAlex.
- miR-484 sensitizes in IDH-wild and IDH-mutant glioblastoma cells to temozolomide by inhibiting oncogenic FOXM1 signaling.Cancer cell international · 2026Article
- RNA Regulatory Networks: Key Hubs in the Panorama of Cancer and Emerging Therapeutic Targets.MedComm · 2026Review
- MicroRNA-based integrated diagnosis and therapy for GBM: current status and advances.Frontiers in immunology · 2026Review
- Exploring the roles and clinical potential of exosome-derived non-coding RNAs in glioma.IBRO neuroscience reports · 2025Review
- Extracellular Vesicles as Mediators and Potential Targets in Combating Cancer Drug Resistance.Molecules (Basel, Switzerland) · 2025Review
- The epigenetic mechanisms involved in the treatment resistance of glioblastoma.Cancer drug resistance (Alhambra, Calif.) · 2025Review
- Epigenetic Downregulation of Hsa-miR-193b-3p Increases Cyclin D1 Expression Level and Cell Proliferation in Human Meningiomas.International journal of molecular sciences · 2023Article
- Forging New Therapeutic Targets: Efforts of Tumor Derived Exosomes to Prepare the Pre-Metastatic Niche for Cancer Cell Dissemination and Dormancy.Biomedicines · 2023Review
- A rationally identified panel of microRNAs targets multiple oncogenic pathways to enhance chemotherapeutic effects in glioblastoma models.Scientific reports · 2022Article
- Dynamic Intercell Communication between Glioblastoma and Microenvironment through Extracellular Vesicles.Biomedicines · 2022Review
- The Role of miRNA in the Pathophysiology of Neuroendocrine Tumors.International journal of molecular sciences · 2021Review
- The Multifaceted Role of Extracellular Vesicles in Glioblastoma: microRNA Nanocarriers for Disease Progression and Gene Therapy.Pharmaceutics · 2021Review
- Exosomal connexin 43 regulates the resistance of glioma cells to temozolomide.Oncology reports · 2021Article
- Review
- Role of Exosomes in Brain Diseases.Frontiers in cellular neuroscience · 2021Review
- The role of extracellular vesicles in acquisition of resistance to therapy in glioblastomas.Cancer drug resistance (Alhambra, Calif.) · 2021Review
- The Role of MicroRNAs in Therapeutic Resistance of Malignant Primary Brain Tumors.Frontiers in cell and developmental biology · 2021Review
- Molecular and Cellular Complexity of Glioma. Focus on Tumour Microenvironment and the Use of Molecular and Imaging Biomarkers to Overcome Treatment Resistance.International journal of molecular sciences · 2020Review
- Review
- Bioinformatics Analysis of Differentially Expressed Genes and miRNAs in Low-Grade Gliomas.Cancer informatics · 2020Article
Corrections and comments
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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
Glioblastoma multiforme (GBM) is a fatal malignancy of the central nervous system, commonly associated with chemoresistance. The alkylating agent Temozolomide (TMZ) is the front-line chemotherapeutic agent and has undergone intense studies on resistance. These studies reported on mismatch repair gene upregulation, ABC-targeted drug efflux, and cell cycle alterations. The mechanism by which TMZ induces cell cycle arrest has not been well-established. TMZ-resistant GBM cells have been linked to microRNA (miRNA) and exosomes. A cell cycle miRNA array identified distinct miRNAs only in exosomes from TMZ-resistant GBM cell lines and primary spheres. We narrowed the miRs to miR-93 and -193 and showed in computational analyses that they could target Cyclin D1. Since Cyclin D1 is a major regulator of cell cycle progression, we performed cause-effect studies and showed a blunting effects of miR-93 and -193 in Cyclin D1 expression. These two miRs also decreased cell cycling quiescence and induced resistance to TMZ. Taken together, our data provide a mechanism by which GBM cells can exhibit TMZ-induced resistance through miRNA targeting of Cyclin D1. The data provide a number of therapeutic approaches to reverse chemoresistance at the miRNA, exosomal and cell cycle points.
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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.