title: XPD could suppress growth of HepG2.2.15 and down-regulate the expression of hepatitis B virus x protein through P53 pathway.
abstract: OBJECTIVE
  We investigated the effects of xeroderma pigmentosum D (XPD) on the growth of hepatoma cells and the expressions of P21, Bax, Bcl-2 and Hepatitis B virus X protein (HBx). In addition, we examined whether XPD affected the aforementioned genes via the P53 pathway.
  
  
  METHODS
  Human hepatoma cells (HepG2.2.15) were transfected with XPD expression vector, followed by incubation with Pifithrin-α (P53 inhibitor). By using RT-PCR and Western blotting, the expression levels of XPD, P53, phospho-P53 (ser-15), P21, Bax, Bcl-2 and HBx were detected. The cell cycle and the apoptosis rate were examined with flow cytometry, and the cell viability was detected by MTT.
  
  
  RESULTS
  Over-expression of XPD up-regulated the expressions of P53, phospho-P53 (ser-15), P21 and Bax but down-regulated the expressions of Bcl-2 and HBx. XPD inhibited the viability of HepG2.2.15 and exacerbated the apoptosis. However, the inhibition of P53 by Pifithrin-α abolished the above-mentioned effects of XPD.
  
  
  CONCLUSIONS
  XPD could suppress growth of hepatoma cells, up-regulate the expressions of P21 and Bax, and down-regulate the expressions of Bcl-2 and HBx through the P53 pathway. There may be mutual influences among XPD, P53 and HBx that co-regulate hepatocarcinogenesis.
authors.affiliation: Department of Gastroenterology, Second Affiliated Hospital, Nanchang University, Nanchang, PR China.
authors.forename: Hao
authors.initials: H
authors.lastname: Ding
authors.forename: Jiang-jing
authors.initials: JJ
authors.lastname: Xu
authors.forename: Yuan
authors.initials: Y
authors.lastname: Huang
authors.forename: Fang-teng
authors.initials: FT
authors.lastname: Du
authors.forename: Ji-xiang
authors.initials: JX
authors.lastname: Zhang
mesh_terms: D052160:Benzothiazoles / Q000494:pharmacology; D006528:Carcinoma, Hepatocellular / Q000378:metabolism / Q000473:pathology*; D049109:Cell Proliferation; D002470:Cell Survival; D015536:Down-Regulation; D056945:Hep G2 Cells; D006801:Humans; D008113:Liver Neoplasms / Q000378:metabolism / Q000473:pathology*; D019253:Proto-Oncogene Proteins c-bcl-2; D016283:Proto-Oncogene Proteins p21(ras) / Q000378:metabolism; D014050:Toluene / Q000031:analogs & derivatives / Q000494:pharmacology; D015534:Trans-Activators / Q000037:antagonists & inhibitors* / Q000378:metabolism; D016159:Tumor Suppressor Protein p53 / Q000037:antagonists & inhibitors / Q000378:metabolism*; D054334:Viral Regulatory and Accessory Proteins; D051759:Xeroderma Pigmentosum Group D Protein / Q000235:genetics / Q000378:metabolism*; D051028:bcl-2-Associated X Protein / Q000378:metabolism
chemical_list: D052160:Benzothiazoles; D019253:Proto-Oncogene Proteins c-bcl-2; D015534:Trans-Activators; D016159:Tumor Suppressor Protein p53; D054334:Viral Regulatory and Accessory Proteins; D051028:bcl-2-Associated X Protein; C057628:hepatitis B virus X protein; D014050:Toluene; C121565:pifithrin; D051759:Xeroderma Pigmentosum Group D Protein; D016283:Proto-Oncogene Proteins p21(ras)