Akademik Veri Yönetim Sistemi
Turkish Journal of Biology, cilt.49, sa.7, ss.800-810, 2025 (SCI-Expanded, Scopus, TRDizin)
Background/aim: Glioblastoma multiforme (GBM) is one of the most aggressive and fatal malignancies of the central nervous system. Despite advancements in treatment strategies, effective therapies for GBM remain insufficient, necessitating further improvements. Notably, miR-22 has been found to be significantly downregulated in both glioblastoma tissues and cell lines. In this study, we aim to evaluate miR-22 expression levels in GBM (U87) and CD133-positive (CD133+) GBM stem cells (GSCs) and to investigate its effects on proliferation, colony formation, migration, invasion, and wound-healing in U87 and CD133+ U87 cells in vitro. Materials and methods: We isolated CD133+ U87 cells using magnetic-activated cell sorting and determined the percentage of CD133+ cells by flow cytometry. qRT-PCR detected miR-22 expression. We transfected miR-22 miRNA into U87, CD133+, and CD133⁻ U87 cells using a lipid-based transfection reagent. Cell viability was assessed spectrophotometrically on days 1, 3, 5, and 7 using the CCK-8 viability assay. Transwell assays were used to analyze migration and invasion. Wound healing was assessed using a scratch assay. Results: MiR-22 expression was lower in CD133+ U87 cells than in U87 cells. MiR-22 overexpression suppressed proliferation in U87, CD133+, and CD133⁻ U87 cells. MiR-22 overexpression also inhibited migration and invasion in both CD133+ and CD133⁻ U87 cells and impaired wound-healing capacity in both U87 and CD133⁻ U87 cells. Conclusion: These results suggest that miR-22 acts as a tumor suppressor in GBM and CD133+ GSCs. Therefore, miR-22 represents a potential therapeutic target for cancer stem cell-based glioblastoma treatment.