ArticleJournal of Cancer2023
miR-21-5p Inhibits the Proliferation, Migration, and Invasion of Glioma by Targeting S100A10.
Article in Journal of Cancer, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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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
13 citing papers in PubMed, 25 citations in OpenAlex.
- BMSC-derived exosomes facilitate osteogenesis and ameliorate ageing-related bone loss through restoring Th17/Treg homeostasis via the miR-21/Skp2/FoxO1 axis.Stem cell research & therapy · 2026Article
- Hypoxia-induced S100A10 promotes glioblastoma malignancy and chemoresistance by activating PI3K-AKT signaling pathway.Functional & integrative genomics · 2025Article
- A new era of cancer immunotherapy: vaccines and miRNAs.Cancer immunology, immunotherapy : CII · 2025Review
- Adiponectin facilitates the cell cycle, inhibits cell apoptosis and induces temozolomide resistance in glioblastoma via the Akt/mTOR pathway.Oncology letters · 2025Article
- Unraveling the noncoding RNA landscape in glioblastoma: from pathogenesis to precision therapeutics.Naunyn-Schmiedeberg's archives of pharmacology · 2024Review
- An novel effective and safe model for the diagnosis of nonalcoholic fatty liver disease in China: gene excavations, clinical validations, and mechanism elucidation.Journal of translational medicine · 2024Article
- VEGFR2 blockade inhibits glioblastoma cell proliferation by enhancing mitochondrial biogenesis.Journal of translational medicine · 2024Article
- Anticancer potential of grifolin in lung cancer treatment through PI3K/AKT pathway inhibition.Heliyon · 2024Article
- MiR-21 Regulates Growth and Migration of Cervical Cancer Cells by RECK Signaling Pathway.International journal of molecular sciences · 2024Article
- Article
- Spatial features of specific CD103Journal of translational medicine · 2024Article
- Identification of Lower Grade Glioma Antigens Based on Ferroptosis Status for mRNA Vaccine Development.Pharmacogenomics and personalized medicine · 2024Article
- Identification of Cuproptosis-Related Genes for Molecular Subtyping: Predicting Prognostic and Therapeutic Response in Glioma.OncoTargets and therapy · 2024Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
S100A10, a member of the S100 protein family, is upregulated in multiple human malignancies and plays a key role in regulating tumor progression. This study aimed to reveal the underlying mechanism by which S100A10 in regulates the proliferation, migration, and invasion of glioma. The expression and clinical information data of S100A10 were downloaded from public databases (TCGA, CGGA, and GEPIA2). S100A10 expression levels in glioma tumor tissues and adjacent nontumor tissues were compared by immunohistochemistry (IHC). The functional roles of S100A10 in glioma were assessed by cell counting kit-8 (CCK-8) cell proliferation assay, wound healing assay, transwell assay, and flow cytometry. miRDB and double luciferase assay were used to predict and identify potential S100A10 mRNA-complementary miRNAs, and the roles of miR-21-5p in glioma cell were examined by targeted knockdown or overexpression miR-21-5p in glioma cell lines. We found that S100A10 was overexpressed in glioma tissues and predicted a worse prognosis. S100A10 knockdown significantly inhibited glioma cell proliferation, invasion, and migration. Furthermore, we demonstrated that miR-21-5p inhibits glioma proliferation, migration, and invasion by targeting S100A10. This study showed S100A10 was a new prognostic predictor among glioma patients and provided new insights into the pathogenesis of gliomas, suggesting that miR-21-5p /S100A10 axis may serve as a valuable therapeutic target for glioma.
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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.