Nuclear factor-kappa B1 inhibits early apoptosis of glioma cells by promoting the expression of Bcl-2.

Glioma is one of the most common types of adult primary brain tumors, and the underlying molecular mechanisms still remain unclear. Nuclear factor-kappa B1 (NF-kappa B1) is involved in a variety of malignancies and is widely expressed in malignant tumors. However, the expression of NF-kappa B1 in different grades of glioma, the correlation between NF-kappa B1 and Bcl-2 expressions in gliomas, and the research between NF-kappa B1 and early apoptosis of glioma cells have not been reported so far. In this study, the expression level of NF-kappa B1 in 31 human glioma tissues and six nonneoplastic brain tissues was determined using quantitative real-time polymerase chain reaction. Results showed that the expression of NF-kappa B1 in human glioma tissues and glioma cell lines, SHG44 and U87, was significantly higher compared to noncancerous brain tissues and that the expression increased with increasing degrees of tumor malignancy. Similar results were demonstrated with the expression of Bcl-2 in the same human glioma specimens. Flow cytometry results showed that inhibition of NF-kappa B1 expression significantly promoted apoptosis of SHG44 and U87 in human glioma cells. Western blot analysis further confirmed decreased expression of Bcl-2 protein after inhibition of NF-kappa B1 protein expression. Taken together, NF-kappa B1 overexpression inhibits early apoptosis of glioma cells and high expression of NF-kappa B1 promotes the expression of antiapoptotic gene Bcl-2. Therefore, our study results provide a theoretical basis for antiapoptotic mechanism of tumor cells in association with NF-kappa B1.