ReviewMolecular neurobiology2021
The Role of the Ubiquitin Proteasome System in Glioma: Analysis Emphasizing the Main Molecular Players and Therapeutic Strategies Identified in Glioblastoma Multiforme.
Review in Molecular neurobiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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
24 citing papers in PubMed, 49 citations in OpenAlex.
- Nanoparticle-Based delivery of proteasome inhibitors for glioblastoma Therapy: Strategies to overcome Blood-Brain barrier and therapeutic resistance.Biochemical pharmacology · 2026Review
- Neuron-glioma synaptic transmission amplified by free 19S proteasome-mediated AMPAR deubiquitination promotes tumor progression.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026Article
- Ubiquitin-Proteasome System-Related Prognostic Model and Immune Landscape in Glioblastoma.International journal of genomics · 2026Article
- Post-translational modifications in DNA damage repair: mechanisms underlying temozolomide resistance in glioblastoma.Oncogene · 2025Review
- Advancing brain tumor therapy: unveiling the potential of PROTACs for targeted protein degradation.Cytotechnology · 2025Review
- Identification of Deregulated miRNAs and mRNAs Involved in Tumorigenesis and Detection of Glioblastoma Patients Applying Next-Generation RNA Sequencing.Pharmaceuticals (Basel, Switzerland) · 2025Article
- UCHL3 induces radiation resistance and acquisition of mesenchymal phenotypes by deubiquitinating POLD4 in glioma stem cells.Cellular and molecular life sciences : CMLS · 2024Article
- The Interplay between Glioblastoma Cells and Tumor Microenvironment: New Perspectives for Early Diagnosis and Targeted Cancer Therapy.Brain sciences · 2024Review
- Shikonin Induces Glioma Necroptosis, Stemness Decline, and Impedes (Immuno)Proteasome Activity.Stem cells international · 2024Article
- Proteasome Inhibitors against Glioblastoma-Overview of Molecular Mechanisms of Cytotoxicity, Progress in Clinical Trials, and Perspective for Use in Personalized Medicine.Current oncology (Toronto, Ont.) · 2023Review
- Role of UBE2C in Brain Cancer Invasion and Dissemination.International journal of molecular sciences · 2023Review
- DUBing Primary Tumors of the Central Nervous System: Regulatory Roles of Deubiquitinases.Biomolecules · 2023Review
- Identification and characterization of putative biomarkers and therapeutic axis in Glioblastoma multiforme microenvironment.Frontiers in cell and developmental biology · 2023Article
- Review
- Biochanin A inhibits lung adenocarcinoma progression by targeting ZEB1.Discover oncology · 2022Article
- Aporphine and isoquinoline derivatives block glioblastoma cell stemness and enhance temozolomide cytotoxicity.Scientific reports · 2022Article
- ONX-0914 Induces Apoptosis and Autophagy with p53 Regulation in Human Glioblastoma Cells.Cancers · 2022Article
- MMP-1, UCH-L1, and 20S Proteasome as Potential Biomarkers Supporting the Diagnosis of Brain Glioma.Biomolecules · 2022Article
- The DNA Double-Strand Break Repair in Glioma: Molecular Players and Therapeutic Strategies.Molecular neurobiology · 2022Review
- Targeted inhibition of ubiquitin signaling reverses metabolic reprogramming and suppresses glioblastoma growth.Communications biology · 2022Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Gliomas constitute the most frequent tumors of the brain. High-grade gliomas are characterized by a poor prognosis caused by a set of attributes making treatment difficult, such as heterogeneity and cell infiltration. Additionally, there is a subgroup of glioma cells with properties similar to those of stem cells responsible for tumor recurrence after treatment. Since proteasomal degradation regulates multiple cellular processes, any mutation causing disturbances in the function or expression of its elements can lead to various disorders such as cancer. Several studies have focused on protein degradation modulation as a mechanism of glioma control. The ubiquitin proteasome system is the main mechanism of cellular proteolysis that regulates different events, intervening in pathological processes with exacerbating or suppressive effects on diseases. This review analyzes the role of proteasomal degradation in gliomas, emphasizing the elements of this system that modulate different cellular mechanisms in tumors and discussing the potential of distinct compounds controlling brain tumorigenesis through the proteasomal pathway.
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What OpenQuestion holds
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.