AI Article Synopsis
- Glioma, specifically glioblastoma (GBM), is a common and severe brain cancer associated with high rates of illness and death, with both exosomes and myeloid-derived suppressor cells (MDSCs) influencing its progression.
- The study aims to examine how exosomal long noncoding RNA AGAP2-AS1 affects the MDSC pathway in GBM, employing various molecular and cellular techniques to analyze gene expression and cell behavior.
- Findings reveal that AGAP2-AS1 is overexpressed in GBM and promotes tumor growth and metastasis by enhancing TGF-β1 expression through a mechanism involving miR-486-3p, suggesting that targeting this pathway could be a new approach for GBM
Article 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.
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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11064146 | PMC |
| http://dx.doi.org/10.1016/j.heliyon.2024.e29949 | DOI Listing |
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