Effect of silencing HMGB1 on epithelial mesenchymal transition of non-small-cell lung cancer

PU Jiangtao; TANG Xiaojun; SONG Qi; HU Zhi; HE Kaiming; WU Yunfei; DAI Tianyang

doi:10.3969/j.issn.1002-266X.2017.36.002

Abstract：Objective To explore the effect of high mobility group box 1 (HMGB1) on epithelial mesenchymal transition (EMT) of non-small-cell lung cancer (NSCLC) and its mechanism.Methods NSCLC A549 cells in the third generation were randomly divided into the si-HMGB1 group,negative control group,and blank group.Cells in the si-HMGB1 group and negative control group were transfected with HMGB1 small interfering RNA (siRNA) sequence,HMGB1 negative control siRNA transfection,and cells in the blank group were not transfected.After 72 h,the HMGB1 silencing efficiency of each group was verified.The expression of EMT-related proteins (E-cadherin,V-cadherin,Vimentin) and signal pathway-related proteins (Snail,NF-κB p65,p-NF-κB p65) in cells collected after 72-hour transfection was detected by Western blotting.Results The expression of HMGB1 mRNA in the si-HMGB1 group was significantly lower than that in the negative control group and blank group (P ＜ 0.05),and there was no significant difference between the negative control group and the blank group (P ＞ 0.05).The protein expression of E-cadherin and VDR of the si-HMGB1 group was significantly higher,and the protein expression of N-cadherin and Vimentin was significantly lower than that of the negative control group and blank group (all P ＜ 0.05),and there was no significant difference between the negative control group and the blank group (P ＞ 0.05).The expression of Snail,p-NF-κB p65 protein of the si-HMGB1 group was lower than that of the negative control group and the blank group (P ＜ 0.05),and there was no significant difference between the negative control group and the blank group (P ＞ 0.05).No significant difference was found in the expression of p-NF-κB p65 among these three groups (all P ＞ 0.05).Conclusion HMGB1 silencing can reverse the EMT process in A549 cells by blocking the Snail/NF-κB signaling pathway.