Glioblastomas (GBM) are highly aggressive brain tumors with limited treatment options, where glioblastoma stem-like cells (GSLCs) pose a major challenge due to their self-renewal capacity, robust DNA repair, and ability to evade immune surveillance. Conventional immunotherapy is often ineffective, making Natural Killer (NK) cells a promising strategy for eradicating therapy-resistant GSLCs. This master’s thesis investigated the Melanoma-Associated Antigen C2 (MAGEC2) protein, identified as a critical factor and potential immunotherapy target. MAGEC2 drives increased GBM malignancy by promoting proliferation and metabolic changes that enhance tumor resistance. To assess MAGEC2’s function, three glioblastoma cell lines expressing the protein were established. We utilized a cytotoxicity assay to analyze the protein’s influence on the interaction with NK cells, and a clonogenic assay to determine its effect on survival following radiotherapy. The results clearly showed that MAGEC2 impacts the sensitivity of glioblastoma cells to NK cell cytotoxicity, suggesting a significant role in anti-tumor immune resistance. Post-radiotherapy data further indicated MAGEC2's involvement in developing radioresistance. Based on these findings, we advocate for further investigation of MAGEC2 as a therapeutic target to develop improved combined strategies. Integrating MAGEC2-targeted therapies with immunotherapy and radiotherapy holds the potential to enhance the overall effectiveness of glioblastoma treatment.
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