Abstract:

Objective To discuss the effect of downregulating of high mobility group box protein 2 （HMGB2） expression on the biological behavior of the liver cancer cells and the epithelial-mesenchymal transition （EMT） process， and to clarify its mechanism. Methods The human liver cancer LM3 cells at logarithmic growth phase were divided into negative control group and HMGB2 RNA interference group （HMGB2 siRNA group）；the cells in two groups were transfected with RNA oligonucleotides（RNA oligos） with irrelevant sequences and RNA oligos designed to knock down HMGB2， and the Lipofectamine 2000 was regarded as the vector.The expression levels of HMGB2 mRNA and protein in the cells in two groups were detected by real-time fluorescence quantitative PCR （RT-qPCR） and Western blotting methods； cell scratch assay and Transwell chamber assay were used to detect the migration and invasion abilities of the cells in two groups； the expression levels of E-cadherin， N-cadherin， and Vimentin proteins and protein kinase B （AKT）/mammalian target of rapamycin （mTOR） pathway related proteins in the cells in two groups were detected by Western blotting method. Results Compared with negative control group， the expression levels of HMGB2 mRNA and protein in the cells in HMGB2 siRNA group were significantly decreased （P<0.05），the cell scratch healing rate was significantly decreased （P<0.01），the number of invasion cells was significantly decreased （P<0.01），and the expression level of E-cadherin protein in the cells was significantly increased （P<0.01）， while the expression levels of N-cadherin， Vimentin， mTOR， AKT， and phosphorylated AKT （p-AKT） proteins in the cells were significantly decreased （P<0.05 or P<0.01）. Conclusion Downregulating the expression of HMGB2 can reduce the migration and invasion abilities of the liver cancer LM3 cells and inhibit the EMT，and its mechanism may be related to regulating the expression of the AKT/mTOR pathway related proteins.

Key words: Liver carcinoma, High mobility group box protein 2, Epithelial-mesenchymal transition, Cell migration, Cell invasion, Protein kinase B/mammalian target of rapamycin