ArticleHeliyon2024
Glioma-derived exosome Lncrna Agap2-As1 promotes glioma proliferation and metastasis by mediating Tgf-β1 secretion of myeloid-derived suppressor cells.
Article in Heliyon, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
15 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Epigenetic reprogramming and antitumor immune responses in gliomas: a systematic review.Medical oncology (Northwood, London, England) · 2025Pooled it
- TGF‑β1 in cancer: From tumour suppressor to promoter, molecular mechanisms, and precision therapeutic strategies (Review).International journal of oncology · 2026Review
- Myeloid-Derived Suppressor Cells: Function, Migration, and Therapeutic Opportunities in Glioblastoma.Cells · 2026Review
- Orchestrating Tumor Metastasis: Exosomes as Master Regulators of the Local and Distant Microenvironment.International journal of biological sciences · 2026Review
- Long non-coding RNAs in the exosomal network: dual roles and clinical implications in cancer.Animal cells and systems · 2026Review
- Microcargos with Megaeffects: A Literature Review of Immunomodulatory, Diagnostic, Prognostic, and Therapeutic Dimensions of Exosomal MicroRNAs in Glioblastoma Multiforme.Cellular and molecular neurobiology · 2025Review
- Exosomal circ_0001583 Drives Glioblastoma Cell Advancement Through the miR-647/CKAP2L Pathway.Molecular neurobiology · 2025Article
- LncRNAs as behind-the-scenes molecules in cancer progression through regulating tumor-associated innate immune system cells.Molecular biology reports · 2025Review
- Exosomes in Glioma: Diagnostic and Therapeutic Potentials.Advances in oncology · 2025Article
- Long Non-Coding RNAs in Malignant Human Brain Tumors: Driving Forces Behind Progression and Therapy.International journal of molecular sciences · 2025Review
- Noncoding RNA-Mediated Regulation of Myeloid-Derived Suppressor Cells in Cancer.Cancer management and research · 2025Review
- Tumor-derived vesicles in immune modulation: focus on signaling pathways.Frontiers in immunology · 2025Review
- Exosomes containing long non-coding RNA AGAP2-AS1 promote the differentiation of CD4Frontiers in genetics · 2025Article
- Exosome-derived circ-001422 promotes tumor-associated macrophage M2 polarization to accelerate the progression of glioma.Communications biology · 2024Article
- Exploring the ceRNA network involving AGAP2-AS1 as a novel biomarker for preeclampsia.Scientific reports · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Glioma (GBM) is the most prevalent malignancy worldwide with high morbidity and mortality. Exosome-mediated transfer of long noncoding RNA (lncRNA) has been reported to be associated with human cancers, containing GBM. Meanwhile, myeloid-derived suppressor cells (MDSCs) play a vital role in mediating the immunosuppressive environments in GBM. Objectives: This study is designed to explore the role and mechanism of exosomal (Exo) lncRNA AGAP2-AS1 on the MDSC pathway in GBM. Methods: AGAP2-AS1, microRNA-486-3p (miR-486-3p), and Transforming growth factor beta-1 (TGF-β1) levels were detected by real-time quantitative polymerase chain reaction (RT-qPCR). Cell proliferation, apoptosis, migration, and invasion were detected by 5-ethynyl-2'-deoxyuridine (EdU), flow cytometry, and Transwell assays. E-cadherin, Vimentin, CD9, CD81, and TGF-β1 protein levels were examined using Western blot. Exosomes were detected by a transmission electron microscope (TEM). Binding between miR-486-3p and AGAP2-AS1 or TGF-β1 was predicted by LncBase or TargetScan and then verified using a dual-luciferase reporter assay. Results: AGAP2-AS1 was highly expressed in GBM tissues and cells. Functionally, AGAP2-AS1 absence or TGF-β1 knockdown repressed tumor cell growth and metastasis. Furthermore, Exo-AGAP2-AS1 from GBM cells regulated TGF-β1 expression via sponging miR-486-3p in MDSCs. Exo-AGAP2-AS1 upregulation facilitated GBM cell growth and metastasis via the MDSC pathway. Conclusion: Exo-AGAP2-AS1 boosted GBM cell development partly by regulating the MDSC pathway, hinting at a promising therapeutic target for GBM treatment.
Indexed as
Identifiers
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.