Oksuz, ErsoyGorgisen, GokhanOzdemir, HulyaGulacar, Ismail MusabOto, Gokhan2025-05-102025-05-1020211019-514910.5137/1019-5149.JTN.27866-19.72-s2.0-85100143725https://doi.org/10.5137/1019-5149.JTN.27866-19.7https://hdl.handle.net/20.500.14720/6937Ozdemir, Hulya/0000-0002-6045-8342AIM: To investigate the relationship between paracetamol and expression levels of cyciooxygenase-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 hours. 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 hours 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.eninfo:eu-repo/semantics/openAccessParacetamolGlioblastomaCox-2Cyclin BApoptosisA172 Glioblastoma CellsEffect of Paracetamol in the Proliferation of Glioblastoma Cell Line: the Role of Apoptosis, Cox-2 and Cyclin B ExpressionsArticle311Q4Q3465033216331WOS:000610243400007