摘要

NF-kappa B signaling pathway plays an important role in carcinogenesis. Although constitutive NF-kappa B activation has been reported in many human tumors, the effect of NF-kappa B signaling pathway in esophageal squamous cell carcinoma (ESCC) is still poorly understood. To explore the role of NF-kappa B signaling pathway in ESCC, RNA interference (RNAi) was used to knockdown the NF-kappa B p65 protein level in the ESCC cells and nude mice. 5-FU was used to investigate whether knockdown NF-kappa B p65 can potentiate 5-FU's antitumor effect. Animal results indicated that tumor growth was inhibited in p65 siRNA and p65 siRNA + 5-FU groups as compared with the control group. Immunohistochemistry, RT-PCR and TUNEL assay showed that p65 siRNA down regulated the expression of p65 and enhanced the sensitivity of EC9706 cells to 5-FU treatment in vivo. Overall, our work indicates that downregulation of p65 can increase tumor apoptosis and potentiates the effects of 5-FU by suppressing NF-kappa B signaling pathway. Thus, p65 is an interesting target for ESCC treatment.