Apoptosis of Gastric Carcinoma SGC7901 Cells Induced by siRNA-mediated Nuclear Factor-kappa B p65 Gene Silencing Combined with 5-Fu

Objective To inhibit the expression of nuclear factor-kappa B(NF-κB)p65 gene in gastric carcinoma SGC7901 cells by siRNA, investigate the effect on cell proliferation and apoptosis and analyze the effect of NF-κB p65 gene on resistance to 5fluorouracil(5-Fu)as a chemotherapeutics. Methods SGC7901 cells were divided into one blank control and four test groups. The cells in four test groups were treated with liposome, 5-Fu, siRNA and 5-Fu + siRNA, while those in blank control group were untreated. The expressions of NF-κB p65 protein in cells of various groups were determined by Western blot, the cell apoptosis by Annexin Ⅴ-PI method, and the cell proliferation level by MTT method. Results The expression levels of NF-κB p65 protein were high in the SGC7901 cells in blank control and liposome groups, while low in 5-Fu, siRNA and 5-Fu + siRNA groups, of which that in 5-Fu + siRNA group was the lowest. The early apoptosis rates of cells in blank control, liposome, 5-Fu, siRNA and 5-Fu + siRNA groups were 1. 40% ± 0. 20%, 2. 36% ± 0. 58%, 6. 68% ± 0. 34%, 6. 60% ± 0. 64% and 21. 62% ± 1. 12% respectively, of which that in 5-Fu + siRNA group was the highest. The proliferation activity of cells decreased with the increasing siRNA concentration and the increasing time for treatment. Conclusion The siRNA inhibited the expression of NF-κB p65 gene effectively, thus inhibited the proliferation and promoted the apoptosis of SGC7901 cells and enhanced the sensitivity of tumor cells to chemotherapeutics.