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AIM: To investigate the mechanism and significance of NF-κB activation regulated by hepatitis B virus X protein (HBx) in hepatitis B virus (HBV)-associated hepatocellular METHODS: The expression levels of HBx, p65,IκB-α and ubiquitin were detected by immunohistochemistry in HCC tissue microarrays (TMA) respevely, and IκB-α was detected RESULTS: The percentage of informative TMA samples was 98.8% in 186 cases with a total of 367 samples. Compared with corresponding liver fissues (60.0%), the HBx expression was obviously decreased in HBV-associated HCC (47.9%,u=2.24, P＜0.05). On the contrary, the expressions of p65 (20.6% vs45.3%, u=4.85, P＜0.01) and ubiquitin (8.9% vs 59.0%, u=9.68, P＜0.01) were notably elevated in HCC. In addition, IκB-α had a tendency to go up. Importantly, positive relativity was observed between HBx and p65 (X2= 10.26,P＜0.01), p65 and IκB-α (X2=16.86, P＜0.01), lκB-α andubiquitin (X2=8.90, P＜0.01) in HCC, respectively.CONCLUSION: Both active and non-active forms of NF-κB are increased in HBV-associated HCC. Variant HBx is the major cause of the enhancement of NF-κB activity. The activation always proceeds in nucleus and the proteasome complexes play an important role in the activation.