RESUMO
Objective To study the effect of hepatitis B vin1s X-interacting protein (HBXIP) on the proliferation,migration,and invasion of ACC-2 cells,and the possible mechanism of the PI3K/Akt signaling pathway involved.Methods The chemically synthesized HBXIP-siRNA plasmid was transfected into the ACC-2 cells.RT-PCR and Western blotting were performed to detect the expression of HBXIP in the ACC-2 cells.Cell proliferation was measured via MTT assay.The invasive and migratory abilities of the ACC-2 cells were evaluated via the transwell chamber assay and scratch test,respectively.Western blotting also detected the impact of HBXIP-siRNA on Akt,p-Akt,PI3K,p-PI3K,and S100A4 protein expression.Results HBXIP was highly expressed and HBXIP-siRNA was successfully transfected in ACC-2 cells.MTT results showed that the number of surviving cells in the experimental group was significantly lower than that in the control group (P＜0.05).The scratch test results showed that the mobility of the experimental group was significantly lower than that of the control group (P＜0.01).The transwell assay showed that the rate of cell invasion of the experimental group was significantly lower than that of the control group (P＜0.01).Finally,Western blotting results revealed that the expression of p-Akt,p-PI3K,and S 100A4 was relatively decreased in the experimental group when compared to that in the control group.Conclusion Silencing the HBXIP gene inhibited ACC-2 proliferation,invasion,and migration.