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Apoptotic induction effect of hepatitis B virus X protein on different hepatocyte lines
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Abstract:
Objective:To study the effect of NF-κB signaling pathway for hepatitis B virus X protein (HBX) on the apoptosis of different hepatocyte lines. Methods: To establish the normal hepatic cell LO2 and hepatic cancer cell HepG2 stably transfected with PEGFP-N1-HBX plasmid (L02/HBX or HepG2/HBX cells). NF-κB signaling pathway inhibitor pyrrolidine dithiocarbamate (PDTC) was used to cut off NF-κB signal transduction in LO2 and HepG2 cells. Flow cytometry was applied to study the cell cycle and apoptosis of LO2 and HepG2 cells before and after PEGFP-N1-HBX transfection as well as before and after PDTC treatment. Western blotting was used to examine the expression of NF-κB. Results: LO2/HBX cells and HepG2/HBX cells stably transfected with PEGFP-N1-HBX were established successfully. The apoptosis of L02/HBX cells significantly increased compared with the control L02 cells \[(31.31±0.51)% vs (14.05±009)%, P<0.05\], and the proportion of cells in G0/G1 stage increased with cells in S and G2/M stage decreased. The apoptosis of HepG2/HBX cells significantly decreased compared with the control HepG2 cells (\[1.21±0.04\]% vs \[1026±0.10\]%, P<0.05), and the proportion of cells in G0/G1 stage decreased with cells in S and G2/M stage increased. After PDTC treatment, the proportion of L02/HBX/PDTC cells in G0/G1 phase increased significantly (\[40.33±0.07\]%), while that in S and G2/M phase decreased remarkably, and the apoptosis rate (\[5.45±007\]%) was at a significantly higher level compared with L02/HBX cells. The apoptosis and the proportion of cells in G0/G1 phase of HepG2/HBX/PDTC were increased significantly, and decreased remarkably in S and G2/M phase, while the apoptosis rate was still lower than the HepG2 cells. The expression of NF-κB protein was significantly decreased in L02/HBX cells but increased in HepG2/HBX cells compared with the control cells. There was almost no expression of NF-κB protein in L02/HBX/PDTC and HepG2/HBX/PDTC cells. Conclusion: HBX can retard the cell cycle of normal hepatic L02 cells and facilitate their apoptosis through down-regulating the expression of NF-κB protein. HBX can accelerate the cell cycle of hepatic cancer HepG2 cells and suppress the apoptosis through up-regulating the expression of NF-κB protein.
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Project Supported:
Project supported by the National Natural Science Foundation of China (No.30672405)
Clc Number:
