Abstract: Abstract Objective：To investigate the effects of xeroderma pigmentosum D(XPD) and P53 on growth of HepG2.2.15, human hepatoma cell, and the expressions of Hepatitis B virus X protein(HBx),Bcl-2 and Bax. Methods: Recombinant plasmid pEGFP-N2/XPD and vacant vector plasmid pEGFP-N2 were transfected into HepG2.2.15 by liposome.On the next day, these cells were incubated with Pifithrin-α,P53 inhibitor, at a 20μM concentration for 24 h. The experiments were divided into five groups: Blank control group;pEGFP-N2 group;pEGFP-N2/XPD group;pEGFP-N2/XPD + Pifithrin-α group;Pifithrin-α group. Through RT-PCR and Western blotting, the expressions of XPD,HBx , Bcl-2and Bax were detected. The cell growth was detected by MTT. The cell cycles were examined with flow cytometry. Results: RT-PCR and Western blotting results showed that the transfection of pEGFP-N2/XPD increased the expression of XPD（P <0.001,respectively）. The increase of XPD expression down-regulated the expressions of HBx and Bcl-2 and up-regulated the expression of Bax, while Pifithrin-α abolished the above-mentioned effects of XPD（P <0.01,respectively）. MTT results showed that the increase of XPD expression inhibited the cell growth and the inhibition of cell growth by XPD was reduced by Pifithrin-α（P <0.001,respectively）. Flow cytometry results showed that the up-regulation of XPD expression increased the cell number of G1 phase and decreased that of S phase, while the effect of XPD on cell cycle was abolished by Pifithrin-α（P <0.001,respectively）. Conclusions: XPD can suppress growth of hepatoma carcinoma cells, down-regulate the expressions of HBx and Bcl-2 and up-regulate the expression of Bax through P53 pathway. There may be mutual influences among XPD, P53 and HBx that co-regulate hepatocarcinogenesis.

Key words: liver neoplasms, carcinoma, cell line tumor, transfection, inhibitor Pifithrin-α, proto-oncogene protein Hepatitis B virus X protein, cell proliferation