Dual Role of Colchicine in Glioblastoma: miR-22-3p-Dependent Regulation of Wound Healing and Proliferation

ABSTRACTObjective: The downregulation of miR-22-3p in glioblastoma (GBM) tissues and cells has been shown to plays a critical role in gliomagenesis and patient prognosis. However, the effects of colchicine on GBM cellular functions via miR-22-3p mediated mechanisms remain unexplored. This study aims to investigate the effects of colchicine on GBM cell behavior through miR-22-3p-mediated mechanisms. Methods: miR-22-3p expression levels were quantified in U87 GBM cells treated with 1, 10, and 100 ng/ml colchicine using qRT-PCR. Cell viability and drug resistance were evaluated using the CCK-8 assay across four groups: temozolomide (TMZ) treated or untreated (i) U87 cells (control), (ii) U87 cells treated with 10 ng/ml colchicine, (iii) U87 cells transfected with a miR-22-3p inhibitor, and (iv) U87 cells transfected with a miR-22-3p inhibitor and 10 ng/ml colchicine. Colony formation was analyzed, migration was assessed using a transwell assay, and wound healing capacity was evaluated via scratch assay, all in U87 cells treated with 10 ng/ml colchicine. Results: Colchicine at 10 ng/ml significantly upregulated miR-22-3p expression. Inhibition of miR-22-3p reversed the colchicine-induced reduction in cell viability and colony formation. Neither colchicine nor miR-22-3p affected the resistance of U87 cells to TMZ. Colchicine reduced U87 cell migration independently of miR-22-3p, while its effect on wound healing was dependent on miR-22-3p expression. Conclusion: This study demonstrates that colchicine modulates miR-22-3p expression and influences key GBM cell functions. These findings provide a preliminary evidence supporting the potential of colchicine as a therapeutic agent in glioblastoma treatment.