In order to elucidate the interference effect of epigallocatechin-3-gallate on targets of nuclear factor κB signal transduction pathway activated by Epstein-Barr virus encoding latent membrane protein 1 in nasopharyngeal carcinoma (NPC) cells, the survival rate of CNE1 and CNE-LMP1 cells after EGCG treatment was determined by MTT assay. NF-κB activation in CNE1 and CNE-LMP1 cells after EGCG treatment was analyzed by promotor luciferase reporter system. And then nuclear translocation in NF-κB（p65）after EGCG treatment was analyzed by immunofluorescence and Western blotting. Meanwhile, the changes of IκBα phosphorylation were observed after EGCG treatment. EGFR promotor activity was analyzed by promotor luciferase reporter system and EGFR phosphorylation was observed by Western blotting after EGCG treatment. It was showed that EGCG inhibited the survival rate of CNE-LMP1 cells and NF-κB activation caused by LMP1 in CNE-LMP1 cells. EGCG also suppressed the nuclear translocation in NF-κB（p65）and IκBα phosphorylation. Meanwhile, EGCG inhibited EGFR promotor activity and EGFR phosphorylation. It can be concluded that EGCG can inhibit NF-κB，NF-κB（p65），IκBα and EGFR which are key targets on NF-κB signal transduction pathway. It was suggested that interference effect of epigallocatechin-3-gallate on signal transduction pathway which activated by LMP1 encoded by EB virus plays an important role in anticancer.