ArticleAging2020
MiR-146b-5p suppresses the malignancy of GSC/MSC fusion cells by targeting SMARCA5.
Article in Aging, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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
16 citing papers in PubMed, 20 citations in OpenAlex.
- MiR-146b-5p/ERBB4 Axis Drives LPS-induced Acute Kidney Injury by Modulating NF-κB/p65.Biochemical genetics · 2026Article
- METTL16-dependent miR-146b-5p m6A modification remodeling sensitize NSCLC to osimertinib via activating PI3K/AKT signaling.BMC cancer · 2025Article
- Article
- Assessment of Expression of lncRNAs in Autistic Patients.Journal of molecular neuroscience : MN · 2024Article
- Molecular Morbidity Score-Can MicroRNAs Assess the Burden of Disease?International journal of molecular sciences · 2024Review
- Upregulation of the ZNF148/PTX3 axis promotes malignant transformation of dendritic cells in glioma stem-like cells microenvironment.CNS neuroscience & therapeutics · 2023Article
- Mutual Regulation of ncRNAs and Chromatin Remodeling Complexes in Normal and Pathological Conditions.International journal of molecular sciences · 2023Review
- Fibroblasts as Turned Agents in Cancer Progression.Cancers · 2023Review
- microRNAs (miRNAs) in Glioblastoma Multiforme (GBM)-Recent Literature Review.International journal of molecular sciences · 2023Review
- LINC01311 exerts an inhibitory effect in thyroid cancer progression by targeting the miR-146b-5p/IMPA2 axis.Translational oncology · 2023Article
- Comparing tumor microRNA profiles of patients with long‑ and short‑term‑surviving glioblastoma.Molecular medicine reports · 2023Article
- Non-coding RNAs and glioma: Focus on cancer stem cells.Molecular therapy oncolytics · 2022Review
- Review
- miR-146b-5p promotes colorectal cancer progression by targeting TRAF6.Experimental and therapeutic medicine · 2022Article
- HELLS serves as a poor prognostic biomarker and its downregulation reserves the malignant phenotype in pancreatic cancer.BMC medical genomics · 2021Article
- Studies on the Regulatory Roles and Related Mechanisms of lncRNAs in the Nervous System.Oxidative medicine and cellular longevity · 2021Review
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recent studies have confirmed that both cancer-associated bone marrow mesenchymal stem cells (BM-MSCs, MSCs) and glioma stem-like cells (GSCs) contribute to malignant progression of gliomas through their mutual interactions within the tumor microenvironment. However, the exact ways and relevant mechanisms involved in the actions of GSCs and MSCs within the glioma microenvironment are not fully understood. Using a dual-color fluorescence tracing model, our studies revealed that GSCs are able to spontaneously fuse with MSCs, yielding GSC/MSC fusion cells, which exhibited markedly enhanced proliferation and invasiveness. MiR-146b-5p was downregulated in the GSC/MSC fusion cells, and its overexpression suppressed proliferation, migration and invasion by the fusion cells. SMARCA5, which is highly expressed in high-grade gliomas, was a direct downstream target of miR-146b-5p in the GSC/MSC fusion cells. miR-146b-5p inhibited SMARCA5 expression and inactivated a TGF-β pathway, thereby decreasing GSC/MSC fusion cell proliferation, migration and invasion. Collectively, these findings demonstrate that miR-146b-5p suppresses the malignant phenotype of GSC/MSC fusion cells in the glioma microenvironment by targeting a SMARCA5-regulated TGF-β pathway.
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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.