EP10.02 A DIABENZALACETONE-BASED COMPOUND MODULATES PROLIFERATION, MIGRATION, AND APOPTOSIS IN MEDULLOBLASTOMA CELLS

Abstract BACKGROUND Medulloblastoma (MB) is a leading cause of cancer-related deaths in children and young adults, accounting for over 20% of paediatric brain tumours. Despite advances in treatment, outcomes remain poor, underscoring the urgent need for novel biomarkers and therapeutic strategies. This study evaluates the therapeutic potential of Dibenzalacetone (DBA) in MB. MATERIAL AND METHODS The half-maximal inhibitory concentration (IC₅₀) of DBA was determined in DAOY cell line using an MTT assay. To evaluate the DBA’s functional effects, cells were treated with DBA at the IC₅₀ concentration, a higher dose (+10 µM), a vehicle control (DMSO), and Cisplatin as a positive control. Cell viability and proliferation were assessed under each condition. Colony formation was quantified, normalised to the DMSO control, and expressed as a percentage relative to untreated controls. The impact of DBA on cell migration was evaluated using a scratch wound healing assay, with wound closure measured at 0, 24, and 48 hours and normalised to DMSO-treated cells. Nuclear morphology and apoptosis-related changes were assessed via DAPI staining, comparing treated and control cells. RESULTS The IC₅₀ of the DBA was determined to be 50 µg/mL. Vehicle control DMSO-treated DAOY cells demonstrated robust colony formation (100%), while DBA at IC₅₀ and the higher concentration reduced colony formation to 36.5% and 35.1%, respectively. The positive control reduced colony formation to 43.3%, indicating comparable efficacy. In wound healing assays, DMSO-treated cells achieved ~100% closure by 48 hours, whereas DBA-treated DAOY cells showed significantly impaired closure, including wound expansion and negative closure percentages at 48 hours. DAPI staining revealed nuclear fragmentation in DBA treated cells, indicating apoptosis, while DMSO-treated cells exhibited intact nuclei and mitotic activity. CONCLUSION The DBA was found to significantly inhibit proliferation, migration, and survival of MB cells, demonstrating strong potential as a therapeutic candidate. Further investigation is warranted to explore its mechanism of action and evaluate its efficacy in paediatric MB cell models.