Aim:Paracetamol has been found to have anti-cancer effects in many studies and these effects have been suggested to be performed by different mechanisms. In this study, we aimed to investigate the relationship between paracetamol and expression levels of cyclooxygenase-2, cyclin B, cell viability and apoptosis in glioblastoma cell line. Material and Methods:The A172 glioblastoma cells were treated with different concentrations of paracetamol and phosphate buffer saline as a vehicle for 24, 48, and 72 h. Cell viability was detected by MTT. Bax, procaspase 3, COX-2 and Cyclin B expressions were detected using Western blotting. Results:A paracetamol treatment of 0.5 mg/mL for 24, 48, and 72 h led to a 14%, 31%, and 37% decrease in cell viability. The expression of COX-2 and cyclin B levels decreased by 36% and 52% respectively, after treatment with 0.5 mg/mL paracetamol. Treatment with 0.5 mg/mL and 1 mg/mL paracetamol significantly induced the expression of cleaved caspase 3, procaspase 3 and Bax proteins compared to the control group (60%, 40%, 21%, %100, 18%, 17%, respectively).Conclusion:The results of our study showed that paracetamol has antitumoral effects on glioblastoma cells and this activity was induced by different signaling pathways.