LPS/TLR4 induces cells EMT through activation of NF-κB. (A) A dual luciferase assay was performed 48 hours after adding LPS. Relative NF-kB luciferase activity, normalized to Renilla luciferase activity, was expressed relative to that of control, set at 1.0. LPS resulted in a significant increase of luciferase activity in SMMC-7721 cells, but had no effect in HepG2 cells; NF-κB inhibitors suppress NF-κB activation in SMMC-7721 cells (*P < 0.05). (B) Immunofluoresence was used to evaluate the NF-κB p65 binding activity of pretreated HepG2 and SMMC-7721 cells. The p65 subunit of NF-κB in the cytosol was stained green and nuclei were stained red with PI (× 400). (C) and (D) qPCR and western-blot were used to detect Snail expression in pretreated HepG2 and SMMC-7721 cells. The results showed that LPS upregulated Snail expression in SMMC-7721 cells, but not in HepG2 cells, NF-κB inhibitors suppress Snail expression in SMMC-7721 cells (* P < 0.05). EMT, epithelial-mesenchymal transition; HCC, hepatocellular carcinoma; LPS, lipopolysaccharide; NF-κB nuclear factor kappa B; TLR4, toll-like receptor 4.