The transfection of SAS cells was performed using jetPEI. SAS cells (2× 10^6 ) were seeded in a 10-cm dish and allowed to grow for 24h. The p-CMV-luc2 vector (8μg) and 16μL of jetPEI solution were diluted with 500μL and 484μL of 145mM NaCl. The mixture was mixed evenly, and incubated at room temperature for 30min. 1000μL jetPEI/DNA mixture was then added to the SAS cells and incubated at 37 °C for 24h.

Oral squamous cell carcinoma often causes bone invasion resulting in poor prognosis and affects the quality of life for patients. Herein, we combined radiation with sorafenib, to evaluate the combination effect on tumor progression and bone erosion in an in situ human OSCC-bearing mouse model. Treatment procedure were arranged as following groups: (a) normal (no tumor); (b) control (with tumor); (c) sorafenib (10 mg/kg/day); (d) radiation (single dose of 6 Gy); (e) pretreatment (sorafenib treatment for 3 days prior to radiation), and (f) concurrent treatment (sorafenib and radiation on the same day). The inhibition of tumor growth and expression level of p65 of NF-kappaB in tumor tissues were the most significant in the pretreatment group. EMSA and Western blot showed that DNA/NF-kappaB activity and the expressions of NF-kappaB-associated proteins were down-regulated. Notably, little to no damage in mandibles and zygomas of mice treated with combination of sorafenib and radiation was found by micro-CT imaging. In conclusion, sorafenib combined with radiation suppresses radiation-induced NF-kappaB activity and its downstream proteins, which contribute to radioresistance and tumorigenesis. Additionally, bone destruction is also diminished, suggesting that combination treatment could be a potential strategy against human OSCC.