ArticleJournal of molecular neuroscience : MN2022
MiR-3918 Inhibits Tumorigenesis of Glioma via Targeting EGFR to Regulate PI3K/AKT and ERK Pathways.
Article in Journal of molecular neuroscience : MN, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed.
- Mutant ribosomal protein RPS15 drives B cell malignancy through oxidative stress and genomic instability.Nature communications · 2026Article
- Innovating Glioma Therapy Using Secretions from Umbilical Cord Mesenchymal Stem Cells to Target Homeobox and Growth Factor Genes.International journal of hematology-oncology and stem cell research · 2025Article
- Mir-338-3p targeting THBS1 attenuates glioma progression by inhibiting the PI3K/Akt pathway.Biology direct · 2024Article
- Identification of Serum miRNAs as Effective Diagnostic Biomarkers for Distinguishing Primary Central Nervous System Lymphoma from Glioma.Journal of immunology research · 2022Article
- BTC as a Novel Biomarker Contributing to EMTFrontiers in genetics · 2022Article
- Long noncoding RNA CCDC183-AS1 depletion represses breast cancer cell proliferation, colony formation, and motility by sponging microRNA-3918.Oncology research · 2021Article
Corrections and comments
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Increasing evidence has demonstrated the miRNAs' action in cancerogenesis and tumor progression. Here, we explored the role and underlying mechanism of miR-3918 during glioma malignancy. miR-3918 and EGFR expression was detected in glioma tissues and tissues by RT-qPCR. The proliferative and migratory rate of glioma cells was assessed through CCK8 and Scratch wound-healing migration assay. Xenograft tumor mouse models were established for in vivo verification. A series of bioinformatics analysis coupled with luciferase reporter assays verified the targeted binding between miR-3918 and EGFR. Expression analyses demonstrated that miR-3918 was poorly expressed in glioma tissues while EGFR abundantly expressed. MiR-3918 overexpression impaired the proliferative and migratory capacities of glioma cells by inactivating PI3K/AKT and ERK pathways. Meanwhile, miR-3918 overexpression also retarded the growth of glioma xenograft. Mechanically, miR-3918 targeted EGFF which was further validated by the correlation of miR-3918 and EGFR expression in glioma tissues. When overexpressed, EGFR can restore the inactivated PI3K/AKT and ERK pathways caused by miR-3918 and influence the glioma cell proliferation and migration. Our findings are the first report that miR-3918/EGFR axis arrested the tumorigenesis of glioma via regulating PI3K/AKT and ERK pathways.
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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.