The medulloblastoma (MB) is the most frequent malignant brain tumour of childhood. Treatment of MB includes surgical tumour resection, radiotherapy, and chemotherapy. Improving the knowledge of tumour biology is fundamental to improve the clinical management of children with MB.A recent study investigated the role of TrkC in MB, a receptor tyrosine kinase whose expression is correlated with a favourable survival outcome. Upon neurotrophin-3 mediated TrkC activation decreased levels of the cytoskeletal protein Cofilin were found.In this study we investigated the role of Cofilin in the cellular functions of MB/cPNET cells. Expression of hemagglutinin-tagged Cofilin in DAOY and PFSK-1 clones led to enhanced proliferation rates when compared to empty-vector (EV) control cells. D425Med clones stably expressing Cofilin showed a decrease in cell motility. Moreover, D425Med Cofilin clones significantly increased their resistance towards cytotoxic drugs and irradiation.To study the underlying mechanism of apoptosis resistance in D425Med clones, we determined the intracellular drug accumulation, the mitochondrial membrane potential, cellular glutathione levels, glutathione-S-transferase activity, and intracellular ATP levels. However, we did not find any alteration when comparing Cofilin and EV-control clones. Using western blot analysis, we found the pro-apoptotic proteins Bad, Bid, caspase 3, caspase 10, and DR5 as well as the anti-apoptotic proteins Bcl-XL, FLIP, and IAP1 to be down-regulated upon Cofilin over-expression. Surprisingly, the pro-apoptotic proteins caspase 7 and HtrA2 revealed an increase in protein levels. The expressional changes of the apoptosis-related proteins may influence the resistance of cells towards cytotoxic agents and irradiation.This thesis proved a role for the Cofilin molecule in the biology of MB, but the question of how Cofilin controls the changes in cellular functions remains to be clarified.