Abstract: Objective To investigate the effect of extracellular histone on epithelial mesenchymal transformation (EMT) and invasion of bladder cancer cells by regulating toll-like receptor 4(TLR4) / nuclear factor-κB (NF-κB) pathway. Methods T24 bladder cancer cells were culturedand divided into 7 groups: control group, histone H3 groups with different concentrations (50, 100, 200 μg / mL), solvent control (0. 1 % DMSO) group, histone H3 (200 μg / mL) + solvent control (0. 1 % DMSO) group, and histone H3 (200 μg / mL) + NF-κB inhibitor Bay11-7082 (10 μmol / L) group. The number of invasion cells and the protein expression levels of E-cadherin, N-cadherin, Vimentin, TLR4 and phosphorylated P65 NF-κB ( p-P65 NF-κB) were detected 24 h after administration. Results The number of invasion cells and the expression levels ofN-cadherin, Vimentin, TLR4 and p-P65 NF-κB in the histone H3 groups were higher than those inthe control group, and the protein expression level of E-cadherin was lower than that in the controlgroup (P < 0. 05), the number of invasion cells and the expression levels of those proteins werechanged with the concentration of histone H3 treatment in a dose-dependent manner. The number ofcell invasion and the protein expression levels of N-cadherin, Vimentin and p-P65 NF-κB in thehistone H3 + Bay11-7082 group were lower than those in the histone H3 + solvent control group,and the expression level of E-cadherin was higher than that in the histone H3 + solvent control group(P< 0. 05). Conclusion Extracellular histone promotes EMT and invasion of bladder cancer cells,which is related to the activation of TLR4 / NF-κB pathway.

Key words: