The role of hepatitis B virus X gene and p53 on hepatocellular carcinoma cell growth.
- Author:
Jing LIN
1
;
Ming-hua ZHU
;
Shi ZHU
;
Jian-hui QU
;
Fang-mei LI
;
Can-rong NI
Author Information
- Publication Type:Journal Article
- MeSH: Apoptosis; Carcinoma, Hepatocellular; pathology; virology; Cell Division; Cell Line, Tumor; Genes, p53; Hepatitis B Antigens; biosynthesis; genetics; Hepatitis B virus; genetics; Humans; Liver Neoplasms; pathology; virology; Trans-Activators; biosynthesis; genetics; Transfection; Tumor Suppressor Protein p53; biosynthesis; genetics
- From: Chinese Journal of Pathology 2003;32(1):43-47
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo explore the effects of hepatitis B virus X gene and p53 on hepatocellular growth.
METHODSTwo kinds of plasmids containing sense and antisense human wild p53 gene respectively were constructed. SMMU-7721 cells were transfected with HBx, sense-wtp53 antisense-wtp53 separately or cotransfected with either HBx and sense-wtp53 or HBx and antisense-wtp53. Flow cytometry was adopted to measure the apoptosis rates and the effects of HBx on cell cycle progression. The activity of p21(Waf1) promoter-luciferase construct was detected. Growth curves for SMMU-7721 stably transfected with pcDNA3 and pcDNA3HBx were analyzed.
RESULTSAfter doxorubicin administration, HBx was noticed able to initiate apoptosis of the liver cells. The apoptosis rate was 5.32% in the pcDNA3 transfected and 12.66% in the pcDNA3HBx transfected groups respectively. HBx could also abrogate p53-mediated apoptosis. The apoptosis rate in groups transfected with pcDNA3, pcDNA3wtp53 and pcDNA3HBx + pcDNA3wtp53 was 5.32%, 11.72% and 4.67% respectively. In compared with the normal group, the number of cells in transiently HBx-expressed group and HBx-transfected group decreased 4.79% and 10.25% respectively. HBx inhibited the activity of p21(Waf1) promoter-luciferase constructed (P < 0.05) and promoted cell growth. The growth rate of HBx expression cells was faster.
CONCLUSIONUnder DNA damage, HBx reduced expression of p21(Waf1) by repressing the activity of p53 protein, followed by disturbing the regulation of G(0)-G(1) cell cycle checkpoint, and promoted the growth rate of hepatoma cells.
