SAS cells (2×10^6) were seeded in a 10-cm dish and allowed to grow for 24 h. The pNF-κBluc2 vector (8 μg) and 16 μl of jetPEI solution were diluted with 500 μl and 484 μl of 145 mM NaCl. The mixture was mixed evenly, and then incubated at room temperature for 30 min. Then, the 1000-μl jetPEI/DNA mixture was added to the SAS cells and incubated at 37˚C for 24 h.

Background/Aim: Although anticancer effects of sorafenib on renal, liver and colon carcinomas are wellknown, its combination effect with ionizing radiation on oral squamous cell carcinoma (OSCC) is unclear. Herein human SAS cells, an OSCC cell line, were used in order to elucidate this combination effect. Materials and Methods: Both SAS and SAS/nuclear factor kappa-B-luciferase (SAS/NF-κBluc2) cell lines were used in the study. Cell viability, NF-κB activation, and protein expression of NF-κB downstream effectors were determined by 3-(4,5-dimethylthiazol-2-yl)2,5-diphenyltetrazolium bromide assay, NF-κB-luc2 reporter gene system, NF-κB/DNA binding activity and western blotting. Results: Sorafenib significantly increased radiationinduced cytotoxicity and apoptosis via both mitochondrialdependent and independent pathways. In addition, NF-κB activity and downstream effector protein expression induced by radiation was suppressed by sorafenib in SAS/NF-κB-luc2 cells. Conclusion: Combination of sorafenib with radiation for the treatment of human OSCC shows a synergistic effect via suppression of radiation-induced NF-κB activity and its regulated downstream effector proteins.