ArticleOncotarget2017
Overexpression of miR-29a reduces the oncogenic properties of glioblastoma stem cells by downregulating Quaking gene isoform 6.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
50 citing papers in PubMed, 77 citations in OpenAlex.
- Increased ATCell death & disease · 2020Trial
- RETRACTION: Downregulation of CRABP2 Inhibit the Tumorigenesis of Hepatocellular Carcinoma in Vivo and in Vitro.BioMed research international · 2026Article
- RETRACTION: Downregulation of CRABP2 Inhibit the Tumorigenesis of Hepatocellular Carcinoma in Vivo and in Vitro.BioMed research international · 2026Article
- Article
- Transcription Factor CEBPD-Mediated WTAP Facilitates the Stemness, Growth, Migration and Glycolysis of Glioblastoma Stem Like Cells.Neurochemical research · 2025Article
- Recent Advances in the Mutual Regulation of m6A Modification and Non-Coding RNAs in Atherosclerosis.International journal of general medicine · 2025Review
- The role of RNA methylation in glioma progression: mechanisms, diagnostic implications, and therapeutic value.Frontiers in immunology · 2025Review
- Uncovering naringin's anticancer mechanisms in glioblastoma via molecular docking and network pharmacology approaches.Scientific reports · 2024Article
- Emerging Roles and Mechanisms of RNA Modifications in Neurodegenerative Diseases and Glioma.Cells · 2024Review
- Use of microRNAs as Diagnostic, Prognostic, and Therapeutic Tools for Glioblastoma.International journal of molecular sciences · 2024Review
- The multifaceted role of quaking protein in neuropsychiatric disorders and tumor progression.Frontiers in neuroscience · 2024Review
- Role of N6-methyladenosine methylation in glioma: recent insights and future directions.Cellular & molecular biology letters · 2023Review
- Insights into the regulatory role of RNA methylation modifications in glioma.Journal of translational medicine · 2023Review
- MicroRNA 29a therapy for CEACAM6-expressing lung adenocarcinoma.BMC cancer · 2023Article
- Multilevel regulation of NGenes & diseases · 2023Review
- The Critical Role of RNA mCellular and molecular neurobiology · 2023Review
- Insights into the Role of LncRNAs and miRNAs in Glioma Progression and Their Potential as Novel Therapeutic Targets.Cancers · 2023Review
- RNA-Binding Proteins in Bladder Cancer.Cancers · 2023Review
- Non-coding RNAs and glioma: Focus on cancer stem cells.Molecular therapy oncolytics · 2022Review
- Molecular Pathways and Genomic Landscape of Glioblastoma Stem Cells: Opportunities for Targeted Therapy.Cancers · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glioblastoma is the most common type of malignant primary brain tumor and has high recurrence and lethality rates. Glioblastoma stem cells (GSCs), a subpopulation of glioblastoma cells, may promote rapid tumor recurrence and therapy resistance. Because altered microRNA (miR) expression in GSCs may lead to glioblastoma progression, we assessed the effects of miR-29a expression on the oncogenic behavior of GSCs. MiR-29a expression was lower in GSCs than non-GSCs, and overexpression of miR-29a in GSCs inhibited cell proliferation, migration and invasion, but promoted apoptosis. MiR-29a directly inhibited the expression of Quaking gene isoform 6 (QKI-6) by binding to its 3'-UTR, and thus inhibited GSC malignant behavior. In addition, Wilms' tumor 1-associating protein (WTAP) was identified as a downstream target of QKI-6. Overexpression of miR-29a in GSCs inhibited expression of WTAP and suppressed both phosphoinositide 3-kinase/AKT and extracellular signal-related kinase pathways by downregulating QKI-6, thereby inhibiting cell proliferation, migration, and invasion but promoting apoptosis. We have characterized a novel miR-29a/QKI-6/WTAP axis in GSCs, which may provide theoretical support for the treatment of glioblastoma with miR-29a agomirs.
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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.