ABSTRACT
Nuclear factor-kappa B (NF-κB) inhibition by NF-κB p65-specific siRNA induced a near-cessation of cell proliferation in EBV-positive stomach cancer cell, and notably diminished cell proliferation in EBV- positive Raji lymphoma cell. In EBV-negative stomach cancer cells, NF-κB inhibition affected variably cell proliferation. Regardless of cell type, NF-κB inhibition suppressed antiapoptotic function of NF-κB, and tended to promote the nuclear accumulation of beta-catenin. This inverse relationship between NF-κB and beta-catenin was evident in 120 resected gastric carcinomas. Conclusively, NF-κB inhibition may be beneficial in the therapy of EBV-positive stomach cancer, but influence variously EBV-negative stomach cancer.